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LU, Yin-Song, Ren-Yu XUE, Guang-Li CAO, Peng-Jie ZHANG, Bo LIU, and Cheng-Liang GONG. "Resistance to BmNPV of Transformation Cells Expressing Short lef-1 dsRNA*." PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS 36, no. 10 (2009): 1356–63. http://dx.doi.org/10.3724/sp.j.1206.2009.00050.
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Mikhailov, Victor S., and George F. Rohrmann. "Baculovirus Replication Factor LEF-1 Is a DNA Primase." Journal of Virology 76, no. 5 (2002): 2287–97. http://dx.doi.org/10.1128/jvi.76.5.2287-2297.2002.
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ABSTRACT The baculovirus replication factors LEF-1 and LEF-2 of the Autographa californica multinucleocapsid nucleopolyhedrovirus were overexpressed as fusions containing a hemagglutinin (HA) epitope and a HIS6 tag using recombinant baculoviruses. LEF-1 was purified to near homogeneity and found to have primase activity in an indirect assay employing Escherichia coli DNA polymerase I (Klenow enzyme) and poly(dT) template. The LEF-1 primase products were also directly characterized by electrophoresis in 20% polyacrylamide-8 M urea gels and agarose gels. Primer synthesis was time dependent, and products of several hundred nucleotides or more were observed from the M13 single-stranded DNA (ssDNA) template. The LEF-1 primase was absolutely dependent on divalent cations (Mg2+), and optimal activity was supported by 10 mM MgCl2. An alkaline pH (8.8 to 9.4) was optimal, whereas monovalent salt (KCl) was inhibitory. Mutation of an invariant aspartic acid in a putative primase domain caused LEF-1 activity to be abolished. Upon ultracentrifugation in glycerol gradients, LEF-1 was found to have a sedimentation coefficient of 3S that is consistent with its being present as a monomer. Elution profiles of LEF-1 and LEF-2 from ssDNA-cellulose and DEAE resin suggested that LEF-2 may bind to both DNA and LEF-1.
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Dunn, S. M., R. A. Keough, G. E. Rogers, and B. C. Powell. "Regulation of a hair follicle keratin intermediate filament gene promoter." Journal of Cell Science 111, no. 23 (1998): 3487–96. http://dx.doi.org/10.1242/jcs.111.23.3487.
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During hair growth, cortical cells emerging from the proliferative follicle bulb rapidly undergo a differentiation program and synthesise large amounts of hair keratin proteins. To identify some of the controls that specify expression of hair genes we have defined the minimal promoter of the wool keratin intermediate filament gene K2.10. The region of this gene spanning nucleotides −350 to +53 was sufficient to direct expression of the lacZ gene to the follicle cortex of transgenic mice but deletion of nucleotides −350 to −150 led to a complete loss of promoter activity. When a four base substitution mutation was introduced into the minimal functional promoter at the binding site for lymphoid enhancer factor 1 (LEF-1), promoter activity in transgenic mice was decreased but specificity was not affected. To investigate the interaction of trans-acting factors within the minimal K2.10 promoter we performed DNase I footprinting analyses and electrophoretic mobility shift assays. In addition to LEF-1, Sp1, AP2-like and NF1-like proteins bound to the promoter. The Sp1 and AP2-like proteins bound sequences flanking the LEF-1 binding site whereas the NF1-like proteins bound closer to the transcription start site. We conclude that the LEF-1 binding site is an enhancer element of the K2.10 promoter in the hair follicle cortex and that factors other than LEF-1 regulate promoter tissue- and differentiation-specificity.
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Kadota, Kanae, Riu Furutani, Amane Makino, Yuji Suzuki, Shinya Wada, and Chikahiro Miyake. "Oxidation of P700 Induces Alternative Electron Flow in Photosystem I in Wheat Leaves." Plants 8, no. 6 (2019): 152. http://dx.doi.org/10.3390/plants8060152.
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Oxygen (O2)-evolving photosynthetic organisms oxidize the reaction center chlorophyll, P700, in photosystem I (PSI) to suppress the production of reactive oxygen species. The oxidation of P700 is accompanied by alternative electron flow in PSI (AEF-I), which is not required for photosynthetic linear electron flow (LEF). To characterize AEF-I, we compared the redox reactions of P700 and ferredoxin (Fd) during the induction of carbon dioxide (CO2) assimilation in wheat leaves, using dark-interval relaxation kinetics analysis. Switching on an actinic light (1000 μmol photons m−2 s−1) at ambient CO2 partial pressure of 40 Pa and ambient O2 partial pressure of 21 kPa gradually oxidized P700 (P700+) and enhanced the reduction rate of P700+ (vP700) and oxidation rate of reduced Fd (vFd). The vFd showed a positive linear relationship with an apparent photosynthetic quantum yield of PSII (Y[II]) originating at point zero; the redox turnover of Fd is regulated by LEF via CO2 assimilation and photorespiration. The vP700 also showed a positive linear relationship with Y(II), but the intercept was positive, not zero. That is, the electron flux in PSI included the electron flux in AEF-I in addition to that in LEF. This indicates that the oxidation of P700 induces AEF-I. We propose a possible mechanism underlying AEF-I and its physiological role in the mitigation of oxidative damage.
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Shanely, R. Andrew, Kevin A. Zwetsloot, Thomas E. Childs, Simon J. Lees, Richard W. Tsika, and Frank W. Booth. "IGF-I activates the mouse type IIb myosin heavy chain gene." American Journal of Physiology-Cell Physiology 297, no. 4 (2009): C1019—C1027. http://dx.doi.org/10.1152/ajpcell.00169.2009.
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IGF-I increases skeletal muscle mass, but whether IGF-I increases type IIb myosin heavy chain (MyHC) transcriptional activity is not known. C2C12 myotubes were cultured with or without IGF-I to determine whether IGF-I increases type IIb MyHC promoter activity, and if so, what region of the promoter might IGF-I signaling regulate. At differentiation days 3 and 4, IGF-I increased type IIb MyHC mRNA and mouse 3.0-kb type IIb MyHC promoter activity. Deletion construct studies identified a potential IGF-I-responsive region between 1.25 and 1.2 kb of the type IIb MyHC promoter, which contained an exact 6-bp T-cell factor/lymphoid enhancer factor (Tcf/Lef) binding site at position −1206 to −1201. Site-specific mutation of the putative Tcf/Lef binding site reduced IGF-I-induced 1.3-kb type IIb MyHC promoter activity. To identify potential IGF-I signaling molecules, the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY-294002 were both found to markedly attenuate IGF-I activation of the 1.3-kb type IIb MyHC promoter. Downstream signaling of IGF-I can phosphorylate and inactivate GSK-3β, thereby enhancing β-catenin protein. The GSK-3β inhibitor, LiCl, dramatically enhanced IGF-I induction of the 1.3-kb type IIb MyHC promoter, and constitutively active GSK-3β attenuated IGF-I-induced 1.3-kb type IIb MyHC promoter activity. Finally, IGF-I increased nuclear β-catenin protein, and small interfering RNA knockdown of β-catenin attenuated IGF-I-induced 1.3-kb type IIb MyHC promoter activity and type IIb MyHC mRNA. In summary, IGF-I stimulation of C2C12 myotubes increases mouse type IIb MyHC promoter activity, likely through signaling of PI3K, GSK-3β, β-catenin, and a Tcf/Lef binding site at −1,206 to −1,201 bp in the promoter.
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Grueneberg, Dorre A., Lourdes Pablo, Kang-Quan Hu, Paul August, Zhigang Weng та Jacqueline Papkoff. "A Functional Screen in Human Cells Identifies UBF2 as an RNA Polymerase II Transcription Factor That Enhances the β-Catenin Signaling Pathway". Molecular and Cellular Biology 23, № 11 (2003): 3936–50. http://dx.doi.org/10.1128/mcb.23.11.3936-3950.2003.
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ABSTRACT β-Catenin signaling plays an important role in the development of many organisms and has a key part in driving the malignant transformation of epithelial cells comprising a variety of cancers. β-Catenin can activate gene expression through its association with transcription factors of the lymphoid enhancer factor 1 (LEF-1)/T-cell factor (TCF) family. We designed a screen in human cells to identify novel genes that activate a β-catenin-LEF/TCF-responsive promoter and isolated the high-mobility group box transcription factor, UBF2. UBF1 and UBF2 are splice variants of a common precursor RNA. Although UBF1 has been shown to activate RNA polymerase I-regulated genes, the function of UBF2 has remained obscure. Here, we show for the first time that both UBF1 and UBF2 activate RNA polymerase II-regulated promoters. UBF2 associates with LEF-1, as shown by coimmunoprecipitation experiments, and potentiates transcriptional activation stimulated by LEF-1/β-catenin from a synthetic promoter with multimerized LEF/TCF binding sites and a natural cyclin D1 promoter with consensus LEF/TCF binding sites. Downregulation of endogenous UBF expression using an RNA interference approach reduces transcriptional activation of a β-catenin-LEF/TCF-responsive promoter by means of overexpressed β-catenin, further implicating UBF as a transcriptional enhancer of the β-catenin pathway.
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Pan, W., Y. Jia, T. Huang, et al. "-catenin relieves I-mfa-mediated suppression of LEF-1 in mammalian cells." Journal of Cell Science 119, no. 23 (2006): 4850–56. http://dx.doi.org/10.1242/jcs.03257.
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Han, Hong, Xumin Cheng, Zhiwei Jia, and K. Alan Shore. "Nonlinear Dynamics of Interband Cascade Laser Subjected to Optical Feedback." Photonics 8, no. 9 (2021): 366. http://dx.doi.org/10.3390/photonics8090366.
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We present a theoretical study of the nonlinear dynamics of a long external cavity delayed optical feedback-induced interband cascade laser (ICL). Using the modified Lang–Kobayashi equations, we numerically investigate the effects of some key parameters on the first Hopf bifurcation point of ICL with optical feedback, such as the delay time (τf), pump current (I), linewidth enhancement factor (LEF), stage number (m) and feedback strength (fext). It is found that compared with τf, I, LEF and m have a significant effect on the stability of the ICL. Additionally, our results show that an ICL with few stage numbers subjected to external cavity optical feedback is more susceptible to exhibiting chaos. The chaos bandwidth dependences on m, I and fext are investigated, and 8 GHz bandwidth mid-infrared chaos is observed.
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Van de Wetering, M., J. Castrop, V. Korinek, and H. Clevers. "Extensive alternative splicing and dual promoter usage generate Tcf-1 protein isoforms with differential transcription control properties." Molecular and Cellular Biology 16, no. 3 (1996): 745–52. http://dx.doi.org/10.1128/mcb.16.3.745.
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Previously, we reported the isolation of cDNA clones representing four alternative splice forms of TCF-1, a T-cell-specific transcription factor. In the present study, Western blotting (immunoblotting) yielded a multitude of TCF-1 proteins ranging from 25-55 kDa, a pattern not simply explained from the known splice alternatives. Subsequent cDNA cloning, PCR amplification, and analysis by rapid amplification of 5' cDNA ends revealed (i) the presence of an alternative upstream promoter, which extended the known N terminus by 116 amino acids, (ii) the presence of four alternative exons, and (iii) the existence of a second reading frame in the last exon encoding an extended C terminus. Inclusion of the extended N terminus into the originally reported protein resulted in a striking similarity to the lymphoid factor Lef-1. Several of the TCF-1 isoforms, although less potent, mimicked Lef-1 in transactivating transcription through the T-cell receptor alpha-chain (TCR-alpha) enhancer. These data provide a molecular basis for the complexity of the expressed TCF-1 proteins and establish the existence of functional differences between these isoforms. Furthermore, the functional redundancy between Tcf-1 and Lef-1 explains the apparently normal TCR-alpha expression in single Tcf-1 or Lef-1 knockout mice despite the firm in vitro evidence for the importance of the Tcf/Lef site in the TCR-alpha enhancer.
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Shimizu, Takehiko, Takahiro Ichinosawa, Yuri Kiguchi, Fusae Ishida, and Takahide Maeda. "<i>Lef</i>1 may contribute to agenesis of the third molars in mice." Open Journal of Stomatology 03, no. 05 (2013): 281–86. http://dx.doi.org/10.4236/ojst.2013.35047.
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Kusano, Shuichi, and Nancy Raab-Traub. "I-mfa Domain Proteins Interact with Axin and Affect Its Regulation of the Wnt and c-Jun N-Terminal Kinase Signaling Pathways." Molecular and Cellular Biology 22, no. 18 (2002): 6393–405. http://dx.doi.org/10.1128/mcb.22.18.6393-6405.2002.
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ABSTRACT I-mfa has been identified as an inhibitor of myogenic basic helix-loop-helix transcription factors, and a related human I-mfa domain-containing protein (HIC) also has been identified as a protein that regulates Tat- and Tax-mediated expression of viral promoters. HIC and I-mfa represent a family of proteins that share a highly conserved cysteine-rich domain, termed the I-mfa domain. We show here that both I-mfa domain proteins, HIC and I-mfa, interacted in vivo with the Axin complex through their C-terminal I-mfa domains. This interaction inhibited Axin-mediated downregulation of free levels of cytosolic β-catenin. I-mfa and HIC also both directly interacted with lymphocyte enhancer factor (LEF); however, I-mfa but not HIC significantly inhibited reporter constructs regulated by β-catenin. The overexpression of HIC but not I-mfa decreased the inhibitory effects of Axin on β-catenin-regulated reporter constructs, while both HIC and I-mfa decreased Axin-mediated c-Jun N-terminal kinase (JNK) activation. These data reveal for the first time that I-mfa domain proteins interact with the Axin complex and affect Axin regulation of both the Wnt and the JNK activation pathways. Interestingly, HIC differs from I-mfa in that I-mfa affects both Axin function and T-cell factor- or LEF-regulated transcription in the Wnt signaling pathway while HIC affects primarily Axin function.
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조규연. "Literary debates between LEF and Constructivism: Poetic Dialogue of V. Mayakovsky and I. Selvinsky." Russian Language and Literature ll, no. 49 (2015): 63–92. http://dx.doi.org/10.24066/russia.2015..49.003.
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van der Vet, Puck C. R., Jip Q. Kusen, Manuela Rohner-Spengler, et al. "Fear of Falling, Recurrence of Falls, and Quality of Life in Patients with a Low Energy Fracture—Part II of an Observational Study." Medicina 57, no. 6 (2021): 584. http://dx.doi.org/10.3390/medicina57060584.
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Background and objective: Falls in elderly cause injury, mortality, and loss of independence, making Fear of Falling (FoF) a common health problem. FoF relates to activity restriction and increased fall risk. A voluntary intervention including fall risk assessment and prevention strategies was implemented to reduce falls in elderly patients with low energy fractures (LEF). The primary purpose of this study was to evaluate FoF and the number of subsequent falls in trauma patients one year after a LEF. The secondary aim was to examine how FoF affects patients’ lives in terms of Quality of Life (QoL), mobility, and activity levels. Finally, participation in the voluntary fall prevention program (FPP) was evaluated. Materials and Methods: Observational cohort study in one Swiss trauma center. LEF patients, treated between 2012 and 2015, were analyzed one year after injury. Primary outcomes were Falls-Efficacy Score-International (FES-I) and number of subsequent falls. Secondary outcomes were EuroQoL-5-Dimensions-3-Levels (EQ5D-3L), mobility, activity levels, and participation in the FPP. Subgroup analysis was performed for different age categories. Results: 411 patients were included for analysis. Mean age was 72 ± 9.3, mean FES-I was 21.1 ± 7.7. Forty percent experienced FoF. A significant negative correlation between FoF and QoL (R = 0.64; p < 0.001) was found. High FoF correlated with lower activity levels (R= −0.288; p < 0.001). Six percent visited the FPP. Conclusions: At follow-up, 40% suffered from FoF which seems to negatively affect patients’ QoL. Nevertheless, participation in the FPP was low. Simply informing patients about their susceptibility to falls and recommending participation in FPPs seems insufficient to motivate and recruit patients into FPPs. We suggest implementing repeated fall risk- and FoF screenings as standard procedures in the follow-up of LEF, especially in patients aged over 75 years.
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Snider, Lauren, Hilary Thirlwell, Jeffrey R. Miller, Randall T. Moon, Mark Groudine, and Stephen J. Tapscott. "Inhibition of Tcf3 Binding by I-mfa Domain Proteins." Molecular and Cellular Biology 21, no. 5 (2001): 1866–73. http://dx.doi.org/10.1128/mcb.21.5.1866-1873.2001.
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ABSTRACT We have determined that I-mfa, an inhibitor of several basic helix-loop-helix (bHLH) proteins, and XIC, a Xenopusortholog of human I-mf domain-containing protein that shares a highly conserved cysteine-rich C-terminal domain with I-mfa, inhibit the activity and DNA binding of the HMG box transcription factor XTcf3. Ectopic expression of I-mfa or XIC in early Xenopus embryos inhibited dorsal axis specification, the expression of the Tcf3/β-catenin-regulated genessiamois and Xnr3, and the ability of β-catenin to activate reporter constructs driven by Lef/Tcf binding sites. I-mfa domain proteins can regulate both the Wnt signaling pathway and a subset of bHLH proteins, possibly coordinating the activities of these two critical developmental pathways.
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Sagun, Julius Ver, Murray R. Badger, Wah Soon Chow, and Oula Ghannoum. "Cyclic electron flow and light partitioning between the two photosystems in leaves of plants with different functional types." Photosynthesis Research 142, no. 3 (2019): 321–34. http://dx.doi.org/10.1007/s11120-019-00666-1.
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Abstract Cyclic electron flow (CEF) around photosystem I (PSI) is essential for generating additional ATP and enhancing efficient photosynthesis. Accurate estimation of CEF requires knowledge of the fractions of absorbed light by PSI (fI) and PSII (fII), which are only known for a few model species such as spinach. No measures of fI are available for C4 grasses under different irradiances. We developed a new method to estimate (1) fII in vivo by concurrently measuring linear electron flux through both photosystems $$\left( {{\text{LEF}}_{{{\text{O}}_{ 2} }} } \right)$$LEFO2 in leaf using membrane inlet mass spectrometry (MIMS) and total electron flux through PSII (ETR2) using chlorophyll fluorescence by a Dual-PAM at low light and (2) CEF as ETR1—$${\text{LEF}}_{{{\text{O}}_{ 2} }}$$LEFO2. For a C3 grass, fI was 0.5 and 0.4 under control (high light) and shade conditions, respectively. C4 species belonging to NADP-ME and NAD-ME subtypes had fI of 0.6 and PCK subtype had 0.5 under control. All shade-grown C4 species had fI of 0.6 except for NADP-ME grass which had 0.7. It was also observed that fI ranged between 0.3 and 0.5 for gymnosperm, liverwort and fern species. CEF increased with irradiance and was induced at lower irradiances in C4 grasses and fern relative to other species. CEF was greater in shade-grown plants relative to control plants except for C4 NADP-ME species. Our study reveals a range of CEF and fI values in different plant functional groups. This variation must be taken into account for improved photosynthetic calculations and modelling.
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Xu, Zhao, Yifeng Sun, Zheng Wei, and Peng Liu. "Suppression of CXCL-1 Could Restore Necroptotic Pathway in Chronic Lymphocytic Leukemia." Blood 134, Supplement_1 (2019): 5466. http://dx.doi.org/10.1182/blood-2019-123748.
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The defective necroptotic pathway and cytokines were important in the pathogenesis and progression of chronic lymphocytic leukemia (CLL). On the other hand, selenite could induce necroptosis in various sold malignancies by generating reactive oxygen species. However, the relationship between necroptosis and cytokines still remains unclear. Here, we managed to clarify the role of different cytokines and selenite in the defective necroptotic pathway of CLL. We first screened the expression of different cytokines related to malignancies between CLL patients and controls using Realtime RT-PCR. Only the expression of CXCL-1, MCP-1, IL-6 and GM-CSF was significantly higher in CLL patients than that of controls. (Figure A, B) In normal B lymphocytes, TNF-α and z-VAD could induce necroptosis and also downregulated the expression of CXCL-1 and MCP-1, which indicated that CXCL-1 and MCP-1 might have correlation with necroptosis. (Figure C) After knockdown of CXCL-1 rather than MCP-1 by siRNA, CLL cells restored the TNF-α/z-VAD induced necroptosis measured by flow cytometry. (Figure D, E) To assess the association between CXCL-1 and lymphoid enhancer-binding factor 1 (LEF-1), which has already been confirmed as the key protein in the necroptotic pathway of CLL, we first performed flow cytometry to verify that CLL cells restored TNF-α/z-VAD induced necroptosis after inhibition of either CXCL-1 or LEF-1. (Figure F) Then, we used Realtime RT-PCR, Western Blot and ELISA to confirm that the expression of LEF-1 was downregulated after inhibiting the expression of CXCL-1 by siRNA, however, the expression of CXCL-1 did not change significantly after knockdown of LEF-1. (Figure G, H, I) This results demonstrated that CXCL-1 located the upstream of LEF-1. To figure out the relationship between cytokines, necroptosis and selenite, we first construct the selenite concentration gradient and selenite with different concentrations was added into CLL cells together with TNF-α and z-VAD. We found that selenite could downregulate the expression of CXCL-1 but had little influence on LEF-1 measured by Realtime RT-PCR. (Figure J) Then, flow cytometry was performed to calculate the percentage of survival CLL cells and only 3.2μM selenite could significantly induce necroptosis of CLL cells. (p = 0.0102, Figure K) Finally, both Western Blot and ELISA showed the similar result that 3.2μM sodium selenite downregulated the translational expression of CXCL-1 but had little impact on LEF-1. (Figure L) Figure Disclosures No relevant conflicts of interest to declare.
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Hernandez-Munain, Cristina, Joseph L. Roberts та Michael S. Krangel. "Cooperation among Multiple Transcription Factors Is Required for Access to Minimal T-Cell Receptor α-Enhancer Chromatin In Vivo". Molecular and Cellular Biology 18, № 6 (1998): 3223–33. http://dx.doi.org/10.1128/mcb.18.6.3223.
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ABSTRACT To understand the molecular basis for the dramatic functional synergy between transcription factors that bind to the minimal T-cell receptor α enhancer (Eα), we analyzed enhancer occupancy in thymocytes of transgenic mice in vivo by genomic footprinting. We found that the formation of a multiprotein complex on this enhancer in vivo results from the occupancy of previously identified sites for CREB/ATF, TCF/LEF, CBF/PEBP2, and Ets factors as well as from the occupancy of two new sites 5′ of the CRE site, GC-I (which binds Sp1 in vitro) and GC-II. Significantly, although all sites are occupied on a wild-type Eα, all sites are unoccupied on versions of Eα with mutations in the TCF/LEF or Ets sites. Previous in vitro experiments demonstrated hierarchical enhancer occupancy with independent binding of LEF-1 and CREB. Our data indicate that the formation of a multiprotein complex on the enhancer in vivo is highly cooperative and that no single Eα binding factor can access chromatin in vivo to play a unique initiating role in its assembly. Rather, the simultaneous availability of multiple enhancer binding proteins is required for chromatin disruption and stable binding site occupancy as well as the activation of transcription and V(D)J recombination.
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Vroon, Ronald. "Aleksei Kruchenykh's "Razboinik Van'ka-Kain" and the Literary Politics of LEF." Slavic Review 50, no. 2 (1991): 359–70. http://dx.doi.org/10.2307/2500211.
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Aleksei Kruchenykh's "Razboinik Van'ka-Kain i Son'ka-manikiurshchitsa" is the first in a cycle of four "crime novels" in verse published by the poet during the heyday of his involvement in postrevolutionary futurist politics. Unlike much of the ephemera he wrote during the 1910s, this particular poem was produced and promoted with unusual care. It first appeared in the sixth, penultimate, issue of Vladimir Maiakovskii's LEF.
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Tomar, Rupal Singh, and Anjana Jajoo. "PSI becomes more tolerant to fluoranthene through the initiation of cyclic electron flow." Functional Plant Biology 44, no. 10 (2017): 978. http://dx.doi.org/10.1071/fp17121.
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Environmental pollution by organic compounds such as polycyclic aromatic hydrocarbons (PAHs) poses a potential ecological risk to photosynthetic organisms. In the present study, the toxic effects of fluoranthene (FLT) on the energy conversion of PSI and PSII in wheat (Triticum aestivum L.) plants were studied. By evaluating the performance of both PSI and PSII, which act as an internal environmental sensor, it was revealed that activity of both photosystems was negatively affected by FLT treatment. However, the quantum yield of PSII, Y(II), was reduced at 5 µM FLT, whereas the quantum yield of PSI, Y(I), significantly decreased at 25 µM FLT. The decline in Y(II) was accompanied by an increase in nonregulated energy dissipation, Y(NO). The decrease in Y(I) induced by FLT was caused by donor-side, and acceptor side limitation of PSI. Cyclic electron flow (CEF) was activated only at higher concentrations and was associated with the inhibition of linear electron flow (LEF) after exposure to a higher concentration of FLT. The inhibition of LEF and induction of CEF seems to be essential for the tolerance of PSI to FLT toxicity.
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Lampart, Alina, Isabelle Arnold, Nina Mäder, et al. "Prevalence of Fractures and Diagnostic Accuracy of Emergency X-ray in Older Adults Sustaining a Low-Energy Fall: A Retrospective Study." Journal of Clinical Medicine 9, no. 1 (2019): 97. http://dx.doi.org/10.3390/jcm9010097.
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Background: Plain radiography (XR) series are standard of care for detection of fall-related fractures in older patients with low-energy falls (LEF) in the emergency department (ED). We have investigated the prevalence of fractures and diagnostic accuracy of XR imaging in the ED. Methods: 2839 patients with LEF, who were presented to two urban level I trauma centers in 2016 and received XR and computed tomography (CT), were consecutively included in this retrospective cohort study. The primary endpoint was the prevalence of fractures of the vertebral column, rib cage, pelvic ring, and proximal long bones. Secondary endpoints were diagnostic accuracy of XR for fracture detection with CT as reference standard and cumulative radiation doses applied. Results: Median age was 82 years (range 65–105) with 64.1% female patients. Results revealed that 585/2839 (20.6%) patients sustained fractures and 452/2839 (15.9%) patients received subsequent XR and CT examinations of single body regions. Cross-tabulation analysis revealed sensitivity of XR of 49.7%, a positive likelihood ratio of 27.6, and negative likelihood ratio of 0.5. Conclusions: XR is of moderate diagnostic accuracy for ruling-out fractures of the spine, pelvic ring, and rib cage in older patients with LEF. Prospective validations are required to investigate the overall risk–benefit of direct CT imaging strategies, considering the trade-off between diagnostic safety, health care costs, and radiation exposure.
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Yamada, Shoya, Hiroshi Ozaki, and Ko Noguchi. "The Mitochondrial Respiratory Chain Maintains the Photosynthetic Electron Flow in Arabidopsis thaliana Leaves under High-Light Stress." Plant and Cell Physiology 61, no. 2 (2019): 283–95. http://dx.doi.org/10.1093/pcp/pcz193.
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Abstract The plant respiratory chain includes the ATP-coupling cytochrome pathway (CP) and ATP-uncoupling alternative oxidase (AOX). Under high-light (HL) conditions, plants experience photoinhibition, leading to a damaged photosystem II (PSII). The respiratory chain is considered to affect PSII maintenance and photosynthetic electron transport under HL conditions. However, the underlying details remain unclear. In this study, we investigated the respiratory chain functions related to PSII maintenance and photosynthetic electron transport in plants exposed to HL stress. We measured the HL-induced decrease in the maximum quantum yield of PSII in the leaves of wild-type and AOX1a-knockout (aox1a) Arabidopsis thaliana plants in which CP was partially inhibited by a complex-III inhibitor. We also calculated PSII photodamage and repair rate constants. Both rate constants changed when CP was partially inhibited in aox1a plants, suggesting that the respiratory chain is related to both processes. Before HL stress, photosynthetic linear electron flow (LEF) decreased when CP was partially inhibited. After HL stress, aox1a in the presence of the CP inhibitor showed significantly decreased rates of LEF. The electron flow downstream from PSII and on the donor side of photosystem I may have been suppressed. The function of respiratory chain is required to maintain the optimal LEF as well as PSII maintenance especially under the HL stress.
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Medici, Damian, та Ali Nawshad. "Type I collagen promotes epithelial–mesenchymal transition through ILK-dependent activation of NF-κB and LEF-1". Matrix Biology 29, № 3 (2010): 161–65. http://dx.doi.org/10.1016/j.matbio.2009.12.003.
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Kleszcz, Robert. "Kanoniczna ścieżka sygnałowa Wnt." Postępy Biochemii 65, no. 3 (2019): 183–92. http://dx.doi.org/10.18388/pb.2019_268.
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Kanoniczna ścieżka sygnałowa Wnt fizjologicznie związana jest z regulacją procesów embriogenezy, różnicowania komórek i ich proliferacji. W transdukcji sygnału uczestniczy wiele białek, z których najważniejszym mediatorem jest β-katenina. W stanie braku pobudzenia ścieżki β-katenina podlega procesowi degradacji proteasomalnej, podczas gdy aktywacja szlaku wiąże się ze wzrostem jej cytoplazmatycznego stężenia i nasileniem translokacji do jądra komórkowego. W wyniku oddziaływania β-kateniny z czynnikami transkrypcyjnymi TCF/LEF dochodzi do zwiększenia ekspresji ponad stu genów docelowych ścieżki Wnt. Nasilenie aktywności kanonicznej ścieżki Wnt obserwuje się w przypadku wielu komórek rakowych, w tym płaskonabłonkowych nowotworów głowy i szyi. Znajomość funkcjonalnej struktury tej ścieżki pozwala z kolei na poszukiwanie terapeutycznych punktów uchwytu w celu zahamowania aktywności transkrypcyjnej β-kateniny w komórkach nowotworowych.
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Sawada, S., and D. R. Littman. "Identification and characterization of a T-cell-specific enhancer adjacent to the murine CD4 gene." Molecular and Cellular Biology 11, no. 11 (1991): 5506–15. http://dx.doi.org/10.1128/mcb.11.11.5506.
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Expression of the CD4 and CD8 glycoproteins is a tightly regulated process tied to the maturation of functionally distinct classes of thymocytes. Therefore, understanding of the mechanism of expression of the genes encoding CD4 and CD8 is likely to yield important insight into regulation of the differentiated functions of T cells. Here, we report the identification of a T-cell-specific enhancer in a DNase I-hypersensitive region about 13 kb 5' of the transcription initiation site of the murine CD4 gene. Within the minimal enhancer element, at least three nuclear protein binding sites were identified by DNase I footprint analysis. One site contains the consensus motif for TCF-1 alpha/LEF-1, a recently identified HMG box transcription factor primarily expressed in pre-B and T cells. By Southwestern (DNA-protein) blotting and binding competition analyses, the protein binding to this site was found to be indistinguishable from TCF-1 alpha/LEF-1. Mutagenesis of this site resulted in loss of factor binding but had a relatively minor effect on enhancer activity. In contrast, mutations in another site, containing two consensus binding motifs for basic helix-loop-helix proteins, abolished factor binding and dramatically reduced enhancer activity. None of the protein binding sites had activity on its own, suggesting that the CD4 enhancer requires the interaction of multiple regulatory sites.
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Sawada, S., and D. R. Littman. "Identification and characterization of a T-cell-specific enhancer adjacent to the murine CD4 gene." Molecular and Cellular Biology 11, no. 11 (1991): 5506–15. http://dx.doi.org/10.1128/mcb.11.11.5506-5515.1991.
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Expression of the CD4 and CD8 glycoproteins is a tightly regulated process tied to the maturation of functionally distinct classes of thymocytes. Therefore, understanding of the mechanism of expression of the genes encoding CD4 and CD8 is likely to yield important insight into regulation of the differentiated functions of T cells. Here, we report the identification of a T-cell-specific enhancer in a DNase I-hypersensitive region about 13 kb 5' of the transcription initiation site of the murine CD4 gene. Within the minimal enhancer element, at least three nuclear protein binding sites were identified by DNase I footprint analysis. One site contains the consensus motif for TCF-1 alpha/LEF-1, a recently identified HMG box transcription factor primarily expressed in pre-B and T cells. By Southwestern (DNA-protein) blotting and binding competition analyses, the protein binding to this site was found to be indistinguishable from TCF-1 alpha/LEF-1. Mutagenesis of this site resulted in loss of factor binding but had a relatively minor effect on enhancer activity. In contrast, mutations in another site, containing two consensus binding motifs for basic helix-loop-helix proteins, abolished factor binding and dramatically reduced enhancer activity. None of the protein binding sites had activity on its own, suggesting that the CD4 enhancer requires the interaction of multiple regulatory sites.
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Xing, Shaojun, Peng Shao, Fengyin Li, et al. "Tle corepressors are differentially partitioned to instruct CD8+ T cell lineage choice and identity." Journal of Experimental Medicine 215, no. 8 (2018): 2211–26. http://dx.doi.org/10.1084/jem.20171514.
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Tle/Groucho proteins are transcriptional corepressors interacting with Tcf/Lef and Runx transcription factors, but their physiological roles in T cell development remain unknown. Conditional targeting of Tle1, Tle3 and Tle4 revealed gene dose–dependent requirements for Tle proteins in CD8+ lineage cells. Upon ablating all three Tle proteins, generation of CD8+ T cells was greatly diminished, largely owing to redirection of MHC-I–selected thymocytes to CD4+ lineage; the remaining CD8-positive T cells showed aberrant up-regulation of CD4+ lineage-associated genes including Cd4, Thpok, St8sia6, and Foxp3. Mechanistically, Tle3 bound to Runx-occupied Thpok silencer, in post-selection double-positive thymocytes to prevent excessive ThPOK induction and in mature CD8+ T cells to silence Thpok expression. Tle3 also bound to Tcf1-occupied sites in a few CD4+ lineage-associated genes, including Cd4 silencer and St8sia6 introns, to repress their expression in mature CD8+ T cells. These findings indicate that Tle corepressors are differentially partitioned to Runx and Tcf/Lef complexes to instruct CD8+ lineage choice and cooperatively establish CD8+ T cell identity, respectively.
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OSChEPKOVA, Olga B., Nicolay А. TSIBULKIN, Elvira B. FROLOVA, and Olga YU MIKhOPAROVA. "r up T ure of lef T V en T r I cular wall as compl I ca TI on of acu T e myocard I al I nfarc TI on. c l I n I cal case." Bulletin of Contemporary Clinical Medicine 5, no. 4 (2012): 31–35. http://dx.doi.org/10.20969/vskm.2012.5(4).31-35.
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Wada, Shinya, Yuji Suzuki, and Chikahiro Miyake. "Photorespiration Enhances Acidification of the Thylakoid Lumen, Reduces the Plastoquinone Pool, and Contributes to the Oxidation of P700 at a Lower Partial Pressure of CO2 in Wheat Leaves." Plants 9, no. 3 (2020): 319. http://dx.doi.org/10.3390/plants9030319.
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The oxidation of P700 in photosystem I (PSI) is a robust mechanism that suppresses the production of reactive oxygen species. We researched the contribution of photorespiration to the oxidation of P700 in wheat leaves. We analyzed the effects of changes in partial pressures of CO2 and O2 on photosynthetic parameters. The electron flux in photosynthetic linear electron flow (LEF) exhibited a positive linear relationship with an origin of zero against the dissipation rate (vH+) of electrochromic shift (ECS; ΔpH across thylakoid membrane), indicating that cyclic electron flow around PSI did not contribute to H+ usage in photosynthesis/photorespiration. The vH+ showed a positive linear relationship with an origin of zero against the H+ consumption rates in photosynthesis/photorespiration (JgH+). These two linear relationships show that the electron flow in LEF is very efficiently coupled with H+ usage in photosynthesis/photorespiration. Lowering the intercellular partial pressure of CO2 enhanced the oxidation of P700 with the suppression of LEF. Under photorespiratory conditions, the oxidation of P700 and the reduction of the plastoquinone pool were stimulated with a decrease in JgH+, compared to non-photorespiratory conditions. These results indicate that the reduction-induced suppression of electron flow (RISE) suppresses the reduction of oxidized P700 in PSI under photorespiratory conditions. Furthermore, under photorespiratory conditions, ECS was larger and H+ conductance was lower against JgH+ than those under non-photorespiratory conditions. These results indicate that photorespiration enhances RISE and ΔpH formation by lowering H+ conductance, both of which contribute to keeping P700 in a highly oxidized state.
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Rhen, Turk, Zachary Even, Alaina Brenner, et al. "Evolutionary Turnover in Wnt Gene Expression but Conservation of Wnt Signaling during Ovary Determination in a TSD Reptile." Sexual Development 15, no. 1-3 (2021): 47–68. http://dx.doi.org/10.1159/000516973.
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Temperature-dependent sex determination (TSD) is a well-known characteristic of many reptilian species. However, the molecular processes linking ambient temperature to determination of gonad fate remain hazy. Here, we test the hypothesis that Wnt expression and signaling differ between female- and male-producing temperatures in the snapping turtle <i>Chelydra serpentina</i>. Canonical Wnt signaling involves secretion of glycoproteins called WNTs, which bind to and activate membrane bound receptors that trigger β-catenin stabilization and translocation to the nucleus where β-catenin interacts with TCF/LEF transcription factors to regulate expression of Wnt targets. Non-canonical Wnt signaling occurs via 2 pathways that are independent of β-catenin: one involves intracellular calcium release (the Wnt/Ca<sup>2+</sup> pathway), while the other involves activation of RAC1, JNK, and RHOA (the Wnt/planar cell polarity pathway). We screened 20 Wnt genes for differential expression between female- and male-producing temperatures during sex determination in the snapping turtle. Exposure of embryos to the female-producing temperature decreased expression of 7 Wnt genes but increased expression of 2 Wnt genes and <i>Rspo1</i> relative to embryos at the male-producing temperature. Temperature also regulated expression of putative Wnt target genes in vivo and a canonical Wnt reporter (6x TCF/LEF sites drive H2B-GFP expression) in embryonic gonadal cells in vitro. Results indicate that Wnt signaling was higher at the female- than at the male-producing temperature. Evolutionary analyses of all 20 Wnt genes revealed that thermosensitive Wnts, as opposed to insensitive Wnts, were less likely to show evidence of positive selection and experienced stronger purifying selection within TSD species.
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Steinbeck, Janina, Ian L. Ross, Rosalba Rothnagel, et al. "Structure of a PSI–LHCI–cyt b6f supercomplex in Chlamydomonas reinhardtii promoting cyclic electron flow under anaerobic conditions." Proceedings of the National Academy of Sciences 115, no. 41 (2018): 10517–22. http://dx.doi.org/10.1073/pnas.1809973115.
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Photosynthetic linear electron flow (LEF) produces ATP and NADPH, while cyclic electron flow (CEF) exclusively drives photophosphorylation to supply extra ATP. The fine-tuning of linear and cyclic electron transport levels allows photosynthetic organisms to balance light energy absorption with cellular energy requirements under constantly changing light conditions. As LEF and CEF share many electron transfer components, a key question is how the same individual structural units contribute to these two different functional modes. Here, we report the structural identification of a photosystem I (PSI)–light harvesting complex I (LHCI)–cytochrome (cyt) b6f supercomplex isolated from the unicellular alga Chlamydomonas reinhardtii under anaerobic conditions, which induces CEF. This provides strong evidence for the model that enhanced CEF is induced by the formation of CEF supercomplexes, when stromal electron carriers are reduced, to generate additional ATP. The additional identification of PSI–LHCI–LHCII complexes is consistent with recent findings that both CEF enhancement and state transitions are triggered by similar conditions, but can occur independently from each other. Single molecule fluorescence correlation spectroscopy indicates a physical association between cyt b6f and fluorescent chlorophyll containing PSI–LHCI supercomplexes. Single particle analysis identified top-view projections of the corresponding PSI–LHCI–cyt b6f supercomplex. Based on molecular modeling and mass spectrometry analyses, we propose a model in which dissociation of LHCA2 and LHCA9 from PSI supports the formation of this CEF supercomplex. This is supported by the finding that a Δlhca2 knockout mutant has constitutively enhanced CEF.
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McGowan, Kevin M., and Pierre A. Coulombe. "Onset of Keratin 17 Expression Coincides with the Definition of Major Epithelial Lineages during Skin Development." Journal of Cell Biology 143, no. 2 (1998): 469–86. http://dx.doi.org/10.1083/jcb.143.2.469.
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The type I keratin 17 (K17) shows a peculiar localization in human epithelial appendages including hair follicles, which undergo a growth cycle throughout adult life. Additionally K17 is induced, along with K6 and K16, early after acute injury to human skin. To gain further insights into its potential function(s), we cloned the mouse K17 gene and investigated its expression during skin development. Synthesis of K17 protein first occurs in a subset of epithelial cells within the single-layered, undifferentiated ectoderm of embryonic day 10.5 mouse fetuses. In the ensuing 48 h, K17-expressing cells give rise to placodes, the precursors of ectoderm-derived appendages (hair, glands, and tooth), and to periderm. During early development, there is a spatial correspondence in the distribution of K17 and that of lymphoid-enhancer factor (lef-1), a DNA-bending protein involved in inductive epithelial–mesenchymal interactions. We demonstrate that ectopic lef-1 expression induces K17 protein in the skin of adult transgenic mice. The pattern of K17 gene expression during development has direct implications for the morphogenesis of skin epithelia, and points to the existence of a molecular relationship between development and wound repair.
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Ly, Tam Minh, Yen-Cheng Chen, Ming-Che Lee, et al. "Snail Upregulates Transcription of FN, LEF, COX2, and COL1A1 in Hepatocellular Carcinoma: A General Model Established for Snail to Transactivate Mesenchymal Genes." Cells 10, no. 9 (2021): 2202. http://dx.doi.org/10.3390/cells10092202.
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SNA is one of the essential EMT transcriptional factors capable of suppressing epithelial maker while upregulating mesenchymal markers. However, the mechanisms for SNA to transactivate mesenchymal markers was not well elucidated. Recently, we demonstrated that SNA collaborates with EGR1 and SP1 to directly upregulate MMP9 and ZEB1. Remarkably, a SNA-binding motif (TCACA) upstream of EGR/SP1 overlapping region on promoters was identified. Herein, we examined whether four other mesenchymal markers, lymphoid enhancer-binding factor (LEF), fibronectin (FN), cyclooxygenase 2 (COX2), and collagen type alpha I (COL1A1) are upregulated by SNA in a similar fashion. Expectedly, SNA is essential for expression of these mesenchymal genes. By deletion mapping and site directed mutagenesis coupled with dual luciferase promoter assay, SNA-binding motif and EGR1/SP1 overlapping region are required for TPA-induced transcription of LEF, FN, COX2 and COL1A1. Consistently, TPA induced binding of SNA and EGR1/SP1 on relevant promoter regions of these mesenchymal genes using ChIP and EMSA. Thus far, we found six of the mesenchymal genes are transcriptionally upregulated by SNA in the same fashion. Moreover, comprehensive screening revealed similar sequence architectures on promoter regions of other SNA-upregulated mesenchymal markers, suggesting that a general model for SNA-upregulated mesenchymal genes can be established.
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Abolade, Jeremiah O., Dominic B. O. Konditi, and Vasant M. Dharmadhikary. "Compact Vitis vinifera-Inspired Ultrawideband Antenna for High-Speed Communications." International Journal of Antennas and Propagation 2021 (May 18, 2021): 1–11. http://dx.doi.org/10.1155/2021/9975884.
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A new compact ultrawideband (UWB) bioinspired antenna is presented in this work. The proposed antenna consists of a vine leaf (Vitis vinifera) shape as the radiating patch, defected ground structure (DGS), and a vertical rectangular slot (VRS) on the ground plane. The vine leaf shape is realized from a circular patch (initiator) in this work. The proposed antenna is built on an FR4 substrate with a dielectric constant of 4.4, a loss tangent of 0.02, and a thickness of 1.5 mm. The total dimension of the proposed bioinspired antenna is 35 × 27.6 mm2. The proposed antenna has a fractional bandwidth of 115.43% (3.7 GHz–13.8 GHz) at 10 dB return loss, a radiation efficiency between 78% and 97%, a peak gain of 6.7 dB, and a stable radiation pattern. The contributions of this work to the existing literature are as follows: (i) the investigation of a vine leaf shape for UWB antenna application; (ii) the adaptation of the conventional monopole patch antenna design equation to determine the lower edge frequency (LEF) of an arbitrary shape monopole antenna; (iii) the presentation of a compact UWB antenna with high fractional bandwidth compared with recent works in the literature, and (iv) the use of FR4 substrate to achieve a peak radiation efficiency of 97% with a compact structure.
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Dal Maso, Luigino, Chiara Panato, Andrea Tavilla, et al. "Cancer cure for 32 cancer types: results from the EUROCARE-5 study." International Journal of Epidemiology 49, no. 5 (2020): 1517–25. http://dx.doi.org/10.1093/ije/dyaa128.
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Abstract Background Few studies have estimated the probability of being cured for cancer patients. This study aims to estimate population-based indicators of cancer cure in Europe by type, sex, age and period. Methods 7.2 million cancer patients (42 population-based cancer registries in 17 European countries) diagnosed at ages 15–74 years in 1990–2007 with follow-up to 2008 were selected from the EUROCARE-5 dataset. Mixture-cure models were used to estimate: (i) life expectancy of fatal cases (LEF); (ii) cure fraction (CF) as proportion of patients with same death rates as the general population; (iii) time to cure (TTC) as time to reach 5-year conditional relative survival (CRS) &gt;95%. Results LEF ranged from 10 years for chronic lymphocytic leukaemia patients to &lt;6 months for those with liver, pancreas, brain, gallbladder and lung cancers. It was 7.7 years for patients with prostate cancer at age 65–74 years and &gt;5 years for women with breast cancer. The CF was 94% for testis, 87% for thyroid cancer in women and 70% in men, 86% for skin melanoma in women and 76% in men, 66% for breast, 63% for prostate and &lt;10% for liver, lung and pancreatic cancers. TTC was &lt;5 years for testis and thyroid cancer patients diagnosed below age 55 years, and &lt;10 years for stomach, colorectal, corpus uteri and melanoma patients of all ages. For breast and prostate cancers, a small excess (CRS &lt; 95%) remained for at least 15 years. Conclusions Estimates from this analysis should help to reduce unneeded medicalization and costs. They represent an opportunity to improve patients’ quality of life.
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Ai, Di, Jun Wang, Melanie Amen, Mei-Fang Lu, Brad A. Amendt, and James F. Martin. "Nuclear Factor 1 and T-Cell Factor/LEF Recognition Elements Regulate Pitx2 Transcription in Pituitary Development." Molecular and Cellular Biology 27, no. 16 (2007): 5765–75. http://dx.doi.org/10.1128/mcb.01848-06.
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ABSTRACT Pitx2, a paired-related homeobox gene that is mutated in Rieger syndrome I, is the earliest known marker of oral ectoderm. Pitx2 was previously shown to be required for tooth, palate, and pituitary development in mice; however, the mechanisms regulating Pitx2 transcription in the oral ectoderm are poorly understood. Here we used an in vivo transgenic approach to investigate the mechanisms regulating Pitx2 transcription. We identified a 7-kb fragment that directs LacZ expression in oral ectoderm and in many of its derivatives. Deletion analysis of transgenic embryos reduced this fragment to a 520-bp region that directed LacZ activity to Rathke's pouch. A comparison of the mouse and human sequences revealed a conserved nuclear factor 1 (NF-1) recognition element near a consensus T-cell factor (TCF)/LEF binding site. The mutation of either site individually abolished LacZ activity in transgenic embryos, identifying Pitx2 as a direct target of Wnt signaling in pituitary development. These findings uncover a requirement for NF-1 and TCF factors in Pitx2 transcriptional regulation in the pituitary and provide insight into the mechanisms controlling region-specific transcription in the oral ectoderm and its derivatives.
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Mainz, Daniela, Ilja Quadt, and Dagmar Knebel-Mörsdorf. "Nuclear IE2 Structures Are Related to Viral DNA Replication Sites during Baculovirus Infection." Journal of Virology 76, no. 10 (2002): 5198–207. http://dx.doi.org/10.1128/jvi.76.10.5198-5207.2002.
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ABSTRACT The ie2 gene of Autographa californica multicapsid nuclear polyhedrosis virus is 1 of the 10 baculovirus genes that have been identified as factors involved in viral DNA replication. IE2 is detectable in the nucleus as one of the major early-expressed proteins and exhibits a dynamic localization pattern during the infection cycle (D. Murges, I. Quadt, J. Schröer, and D. Knebel-Mörsdorf, Exp. Cell Res. 264:219-232, 2001). Here, we investigated whether IE2 localized to regions of viral DNA replication. After viral DNA was labeled with bromodeoxyuridine (BrdU), confocal imaging indicated that defined IE2 domains colocalized with viral DNA replication centers as soon as viral DNA replication was detectable. In addition, a subpopulation of IE2 structures colocalized with two further virus-encoded replication factors, late expression factor 3 (LEF-3) and the DNA binding protein (DBP). While DBP and LEF-3 structures always colocalized and enlarged simultaneously with viral DNA replication sites, only those IE2 structures that colocalized with replication sites also colocalized with DBP. Replication and transcription of DNA viruses in association with promyelocytic leukemia protein (PML) oncogenic domains have been observed. By confocal imaging we demonstrated that the human PML colocalized with IE2. Triple staining revealed PML/IE2 domains in the vicinity of viral DNA replication centers, while IE2 alone colocalized with early replication sites, demonstrating that PML structures do not form common domains with viral DNA replication centers. Thus, we conclude that IE2 colocalizes alternately with PML and the sites of viral DNA replication. Small ubiquitin-like modifier SUMO-1 has been implicated in the nuclear distribution of PML. Similar to what was found for mammalian cells, small ubiquitin-like modifiers were recruited to PML domains in infected insect cells, which suggests that IE2 and PML colocalize in conserved cellular domains. In summary, our results support a model for IE2 as part of various functional sites in the nucleus that are connected with viral DNA replication.
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Alachkar, Houda, Kati Maharry, Ramasamy Santhanam, et al. "SPARC contributes to Leukemia Growth and Aggressive Disease in Acute Myeloid Leukemia (AML)." Blood 120, no. 21 (2012): 773. http://dx.doi.org/10.1182/blood.v120.21.773.773.
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Abstract Abstract 773 Altered expression of SPARC, [secreted protein, acidic, cysteine-rich (osteonectin)] a gene encoding a protein that modulates cell-matrix interactions, has been reported in cancer and leukemia, but its precise contribution to malignant transformation is unknown. We previously reported that SPARC was among the most upregulated genes in the gene-expression profile (GEP) associated with IDH2-R172 mutations (mut; Marcucci et al. JCO 2010;28:2348) and among the most downregulated genes associated with NPM1 mut (Becker et al. JCO 2010;28:596) in cytogenetically normal (CN) AML. Both mutations have strong but opposite impact (IDH2-R172 mut, adverse; NPM1 mut, favorable) on clinical outcome. Thus, we hypothesized that SPARC may act as an oncogene and contribute to AML aggressiveness. To determine functional and mechanistic activities of SPARC in AML, we conducted gain- and loss-of-function experiments in cell lines and primary blasts collected from patients under the OSU Leukemia Tissue Bank protocol. In vitro, ectopic expression and knockdown of SPARC in THP-1 and Kasumi-1 AML cells led to increase (2.5-fold P=0.03) and decrease (45%, P=0.03) in colony forming ability, respectively. Clonogenic assays in SPARC- vs empty vector (EV)-infected AML blasts also showed 2-fold increase in colony-formation (P=.01) supporting a role of SPARC overexpression in promoting leukemia growth. The leukemogenic activity of the SPARC protein was likely mediated by its binding to αvβ3 integrin and in turn by the activation of the kinase ILK. This induced GSK3β phosphorylation (p) and in turn activation of β-catenin, previously reported to contribute to AML. Indeed, while ILK knockdown abolished SPARC-induced p-GSK3β, ectopic SPARC expression led to a 4-fold increased p-GSK3β, measured by p-GSK3β (Ser-9) immunoblot assay, and to stabilization of β-catenin, measured by p-β-catenin(Ser-552) and p-β-catenin(Ser-675) immunoblot assays in AML blasts. As a result, we observed increase in translocation of β-catenin to the nucleus in SPARC overexpressing cells by confocal microscopy. Nuclear β-catenin led to increased activity of the TCF/LEF transcription factors as shown by a TCF/LEF luciferase reporter assay (5.8-fold, P<.001) and the expression of MYC, a TCF/LEF target gene. In contrast, SPARC knockdown decreased MYC expression (50%; P=0.05) in AML blasts. In vivo, mice engrafted with THP-1 cells overexpressing SPARC exhibit more aggressive disease, significant splenomegaly (P=.008), and hepatomegaly with increased number and size of hepatic granulocytic sarcoma-like lesions when compared with mice engrafted with THP-1-EV cells. The results in the preclinical models prompted us to evaluate whether higher SPARC expression associated with aggressive human disease. Thus, SPARC expression levels were measured by NanoString nCounter assay in a cohort of CN-AML patients (pts; n=362; age, 18–83 years) comprehensively characterized for mutations in the NPM1, FLT3, CEBPA, WT1, TET2, MLL, IDH1, IDH2, RUNX1, ASXL1 and DNMT3A genes, and treated with cytarabine-anthracycline based regimens. Higher SPARC expressers were more likely classified in the European Leukemia Net (ELN) Intermediate-I (CEBPA wt, NPM1 mut with FLT3-ITD, or NPM1 wt) than the ELN Favorable Genetic Group (CEBPA mut and/or NPM1 mut without FLT3-ITD; P<.001). Higher expression of SPARC associated with lower complete remission (CR) rates (P<.001; OR .75), shorter disease-free (DFS; P<.001; HR 1.17) and overall (OS; P<.001; HR 1.16) survival. In multivariable analyses, higher SPARC expression remained associated with worse CR rates (P<.001), once adjusted for RUNX1, white blood count (WBC) and age group (<60 vs >60 years); shorter DFS (P=.07), once adjusted for FLT3-ITD, RUNX1, WBC and age group; and shorter OS (P<.001), once adjusted for FLT3-ITD, WT1, ASXL1 and age group. Gene and microRNA (miR)-expression profiling associated SPARC with CD34, BAALC and MN1 among the most upregulated and the HOX genes among the most downregulated genes, and with the hematopoietic stem cell-specific miR-126 and miR-130a among the most upregulated miRs. In conclusion, high SPARC expression contributes to aggressive AML growth via β-catenin activation-mediated mechanisms. SPARC overexpression independently predicted worse outcome in CN-AML pts, and may represent a potentially novel prognostic marker and therapeutic target in AML. Disclosures: No relevant conflicts of interest to declare.
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Patel, Maulin Mukeshchandra, Robert Silasi-Mansat, Ravi Shankar Keshari, et al. "Role of Androgen Dependent TFPI-Regulating Protein (ADTRP) in Vascular Development and Function." Blood 128, no. 22 (2016): 556. http://dx.doi.org/10.1182/blood.v128.22.556.556.
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Abstract We used in vitro and in vivo models to characterize the physiological role of the novel protein encoded by C6ORF105. This gene's expression is androgen-responsive, and the encoded protein is predicted to be palmitoylated and membrane multi-spanning. Previously we showed that C6ORF105 expression co-regulates with tissue factor pathway inhibitor (TFPI)in human endothelial cells (EC); hence we named this protein "androgen-dependent TFPI-regulating protein" (ADTRP). Using in vitro cell-based TOP-Flash reporter assay we identified ADTRP as a negative regulator of canonical Wnt signaling in human cells. Overexpressing ADTRP in HEK293T cells inhibited the activity of beta-catenin/TCF-dependent transcriptional reporter, while silencing ADTRP increased the expression of Wnt target genes LEF-1, AXIN-2, IL-8 and DKK-2 in EA.hy926 EC line and HUVEC. Addition of LiCl showed that the effect of ADTRP was upstream of GSK3, therefore we focused the investigations on the Wnt signalosome proteins. ADTRP expression in HEK293T cells led to decreased phosphorylation of Wnt co-receptor LRP6, suggesting that ADTRP can affect this critical membrane-located event of Wnt signaling. Furthermore, ADTRP expression in reporter cells transfected with a constitutively phosphorylated form of LRP6 (LRP6DN mutant) inhibited Wnt3a- induced signaling, which suggests that ADTRP can interfere with events downstream of LRP6 phosphorylation, such as Axin-2 binding. Altogether, these data indicate that the Wnt signaling inhibitory activity of ADTRP takes place at the plasma membrane level. Site directed mutagenesis of the predicted palmitoylation site Cys61 showed that Wnt inhibitory effects of ADTRP require palmitoyl-mediated anchoring, highlighting the importance of proper membrane location of ADTRP for Wnt pathway inhibition. In vivo morpholino-based knockdown of adtrp in zebrafish embryos produced aberrant angiogenesis, defective branching and ruptured vessels, hemorrhage spots, pericardial edema and slow heart-beat, all reminiscent of defects caused by activation of canonical Wnt signaling. Indeed, adtrp knock down increased Wnt mediated lef-1 and pax-2a as well as mmp2 and mmp9 mRNA expression. Co-injection of ADTRP mRNA partially recovered the adtrp morpholino- induced morphologic abnormalities. Also, knock down of adtrp in a Wnt reporter zebrafish showed increased expression of ectopic Wnt signaling. Furthermore, our recently established Adtrp-/- mice also display some typical Wnt-mediated vascular defects, including: (i) abnormal patterning, increased capillary tortuosity, abnormal branching and increased density of the capillary network; (ii) dilated vessels, especially venules and veins; (iii) increased leakeage of permeability tracers (Evans blue and fluorescent dextran) without evident changes in endothelial junctions; (iv) hemorrhage spots in the skin, meningeal layers, heart, bladder and kidneys; (v) intravascular and interstitial fibrin deposition in the lung, liver and kidney. ADTRP deficiency decreased plasma TFPI antigen by ~2-times. Furthermore, TFPI antigen and anticoagulant activity in lung extracts and isolated lung EC were similarly decreased, which confirms our previous in vitro data. We aslo noticed increased tail bleeding time (>500 sec vs. 200 sec in WT littermates) and blood volume loss, which likely was caused by increased dilation of the tail vein. Gene expression analysis of whole organs showed upregulation of Wnt target genes involved in vascular contractility (Nos3), and extracellular matrix remodeling (Mmp2). Similarly, skin fibroblasts and lung EC isolated from Adtrp-/- mice showed increased expression of Wnt target genes (Lef-1, Cyclin D, Dkk2, c-Myc), which indicates constitutive activation of canonical Wnt signaling. In conclusion, we used genetic animal models and cell culture systems to show for the first time that the novel protein ADTRP plays major roles in vascular development and function. Lack of, or low levels of ADTRP associate with activation of coagulation and vascular development defects, which may be due, at least in part, to intrinsic high levels of ectopic canonical Wnt signaling. Disclosures No relevant conflicts of interest to declare.
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Deng, Fei, Ranran Wang, Minggang Fang, et al. "Proteomics Analysis of Helicoverpa armigera Single Nucleocapsid Nucleopolyhedrovirus Identified Two New Occlusion-Derived Virus-Associated Proteins, HA44 and HA100." Journal of Virology 81, no. 17 (2007): 9377–85. http://dx.doi.org/10.1128/jvi.00632-07.
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ABSTRACT Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and mass spectrometry were used to analyze the structural proteins of the occlusion-derived virus (ODV) of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus (HearNPV), a group II NPV. Twenty-three structural proteins of HearNPV ODV were identified, 21 of which have been reported previously as structural proteins or ODV-associated proteins in other baculoviruses. These include polyhedrin, P78/83, P49, ODV-E18, ODV-EC27, ODV-E56, P74, LEF-3, HA66 (AC66), DNA polymerase, GP41, VP39, P33, ODV-E25, helicase, P6.9, ODV/BV-C42, VP80, ODV-EC43, ODV-E66, and PIF-1. Two proteins encoded by HearNPV ORF44 (ha44) and ORF100 (ha100) were discovered as ODV-associated proteins for the first time. ha44 encodes a protein of 378 aa with a predicted mass of 42.8 kDa. ha100 encodes a protein of 510 aa with a predicted mass of 58.1 kDa and is a homologue of the gene for poly(ADP-ribose) glycohydrolase (parg). Western blot analysis and immunoelectron microscopy confirmed that HA44 is associated with the nucleocapsid and HA100 is associated with both the nucleocapsid and the envelope of HearNPV ODV. HA44 is conserved in group II NPVs and granuloviruses but does not exist in group I NPVs, while HA100 is conserved only in group II NPVs.
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Scheller, E. L., J. Chang та C. Y. Wang. "Wnt/β-catenin Inhibits Dental Pulp Stem Cell Differentiation". Journal of Dental Research 87, № 2 (2008): 126–30. http://dx.doi.org/10.1177/154405910808700206.
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Dental pulp stem cells (DPSCs) are a unique precursor population isolated from postnatal human dental pulp and have the ability to regenerate a reparative dentin-like complex. Canonical Wnt signaling plays a critical role in tooth development and stem cell self-renewal through β-catenin. In this study, the regulation of odontoblast-like differentiation of DPSCs by canonical Wnt signaling was examined. DPSCs were stably transduced with canonical Wnt-1 or the active form of β-catenin, with retrovirus-mediated infection. Northern blot analysis found that Wnt-1 strongly induced the expression of matricellular protein osteopontin, and modestly enhanced the expression of type I collagen in DPSCs. Unexpectedly, Wnt-1 inhibited alkaline phosphatase (ALP) activity and the formation of mineralized nodules in DPSCs. Moreover, over-expression of β-catenin was also sufficient to suppress the differentiation and mineralization of DPSCs. In conclusion, our results suggest that canonical Wnt signaling negatively regulates the odontoblast-like differentiation of DPSCs. Abbreviations used: DPSC, dental pulp stem cell; ALP, alkaline phosphatase; BSP, bone sialoprotein; MSC, mesenchymal stem cell; β-GP, β-glycerophosphate; APC, adenomatous polyposis coli; GSK-3β, glycogen synthase kinase-3β; LRP, LDL receptor-related protein; Tcf, T-cell factor; LEF, lymphoid enhancer factor; FCS, fetal calf serum; AA, L-ascorbic acid 2-phosphate; α-MEM, α-modified Eagle’s medium; PBS, phosphate-buffered saline; HA, hemagglutinin; ON, osteonectin; OPN, osteopontin.
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Mikhailov, Victor S., Alla L. Mikhailova, Masashi Iwanaga, Sumiko Gomi, and Susumu Maeda. "Bombyx mori Nucleopolyhedrovirus Encodes a DNA-Binding Protein Capable of Destabilizing Duplex DNA." Journal of Virology 72, no. 4 (1998): 3107–16. http://dx.doi.org/10.1128/jvi.72.4.3107-3116.1998.
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ABSTRACT A DNA-binding protein (designated DBP) with an apparent molecular mass of 38 kDa was purified to homogeneity from BmN cells (derived fromBombyx mori) infected with the B. morinucleopolyhedrovirus (BmNPV). Six peptides obtained after digestion of the isolated protein with Achromobacter protease I were partially or completely sequenced. The determined amino acid sequences indicated that DBP was encoded by an open reading frame (ORF16) located at nucleotides (nt) 16189 to 17139 in the BmNPV genome (GenBank accession no. L33180 ). This ORF (designated dbp) is a homolog of Autographa californica multicapsid NPV ORF25, whose product has not been identified. BmNPV DBP is predicted to contain 317 amino acids (calculated molecular mass of 36.7 kDa) and to have an isoelectric point of 7.8. DBP showed a tendency to multimerization in the course of purification and was found to bind preferentially to single-stranded DNA. When bound to oligonucleotides, DBP protected them from hydrolysis by phage T4 DNA polymerase-associated 3′→5′ exonuclease. The sizes of the protected fragments indicated that a binding site size for DBP is about 30 nt per protein monomer. DBP, but not BmNPV LEF-3, was capable of unwinding partial DNA duplexes in an in vitro system. This helix-destabilizing ability is consistent with the prediction that DBP functions as a single-stranded DNA binding protein in virus replication.
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Zhang, Jianhua, Renée Lapointe, David Thumbi, Benoit Morin, and Christopher J. Lucarotti. "Molecular comparisons of alphabaculovirus-based products: Gypchek with Disparvirus (Lymantria dispar) and TM BioControl-1 with Virtuss (Orgyia pseudotsugata)." Canadian Entomologist 142, no. 6 (2010): 546–56. http://dx.doi.org/10.4039/n10-037.
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AbstractGypsy moth, Lymantria dispar (L.) (Lepidoptera: Lymantriidae), multicapsid nucleopolyhedrovirus (LdMNPV) has been registered as a microbial pest-control product in the United States (Gypchek®) and Canada (Disparvirus®). Similarly, Douglas-fir tussock moth, Orgyia pseudotsugata (McDunnough) (Lepidoptera: Lymantriidae), multicapsid nucleopolyhedrovirus (OpMNPV) is registered in the United States and Canada as TM BioControl-1® and a product derived from TM BioControl-1 (Virtuss®) is also registered in Canada. To determine changes that may have occurred in these products over time, we compared DNA from Gypchek with Disparvirus and DNA from TM BioControl-1 with Virtuss using restriction fragment length polymorphism (RFLP) analysis. Gypchek and Disparvirus showed the same RFLP banding patterns when viral genomic DNA was digested with BamH I, EcoR V, and Hind III and only a single band difference at approximately 1.6 kilobase (kb) when digested with Bgl II. TM BioControl-1 and Virtuss showed no differences in genomic DNA when digested with Bgl II, Sam I or Hind III. Twelve viral open reading frames (ORFs) were amplified from Gypchek and Disparvirus and nine from TM BioControl-1 and Virtuss by polymerase chain reactions (PCR). The amplified ORFs ranged from highly conserved (polyhedrin) to least conserved (vp91 capsid associated protein). The products were sequenced and the deduced protein products compared. Amino acid sequences deduced from the sequenced PCR products indicated that 8 of the 12 proteins were identical in the two LdMNPV products. The four proteins showing minor sequence variations were DNA polymerase, LEF-8, P74 envelope protein, and VP 91 capsid associated protein. No differences were detected in the protein products deduced from the nine sequenced ORFs from TM BioControl-1 and Virtuss. Comparative RFLP and protein phylogenetic analyses of Gypchek with Disparvirus and TM BioControl-1 with Virtuss revealed little difference between the respective LdMNPV and OpMNPV populations that make up these product pairs.
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Bungartz, Gerd, Russell Garrett, and Stephen G. Emerson. "NF-Ya Is Essential for Hematopoieic Stem Cell Proliferation." Blood 114, no. 22 (2009): 1507. http://dx.doi.org/10.1182/blood.v114.22.1507.1507.
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Abstract Abstract 1507 Poster Board I-530 Proliferation, self-renewal and differentiation of hematopoietic stem cells (HSCs) must be tightly regulated in order to sustain hematopoiesis over a lifetime and to prevent uncontrolled expansion of cells. Several genes have been implicated in the regulation of HSC behavior, such as HoxB4, Notch1, Lef-1 and others. Previous studies from our and other laboratories have demonstrated that the heterotrimeric transcription factor NF-Y is a potent inducer of many of these regulatory genes by over-expressing NF-Ya, the regulatory subunit of NF-Y. Furthermore, Bhattarchaya et al. showed that the deletion of NF-Ya in mice leads to lethality before day E8.5, highlighting its importance in mouse development. While there is no doubt that NF-Y plays a role in the progression of the cell cycle in vitro, different groups – targeting different subunits for deletion or silencing – have obtained different results. In order to comprehensively investigate the in vivo function of NF-Y in the hematopoietic system, we utilized a conditional knockout mouse model. We found that the bone marrow (BM) cellularity decreases sharply starting as soon as one day after the ablation of NF-Ya. Our data indicate that the cell loss can be attributed to a combination of cell cycle arrest in G2/M-phase of the cell cycle and apoptosis at 24 hours after the gene deletion. Since NF-Y has been identified as a master regulator of genes involved in HSCs behavior, we focused on the effects of the NF-Ya deletion within the HSC compartment. We found a down regulation of HoxB4, Notch-1, Lef-1 and Bmi-1 following NF-Ya deletion. However, 24h after induction of NF-Ya deletion the HSC population appeared unaffected and their numbers remained stable, likely due to their predominantly quiescent status. To investigate the capability of stem cells to progress though the cell cycle, we activated HSCs using the interferon inducer poly IC and observed that, once activated, also HSCs accumulate in the G2/M-phase of the cell cycle. Finally, to test whether the deletion of NF-Ya impairs or absolutely abrogates HSC function, we performed long term experiments including competitive BM transplantation and colony formation assays that demonstrate that NF-Y activity is absolutely essential for HSC function. Altogether, our data identify NF-Y plays a pivotal role in the survival of hematopoietic cells and the progression of cells though the G2/M-phase of the cell cycle in vivo. Additionally, while we found that NF-Y ablation leads to reduced expression of many genes important for HSC behavior, this had no immediate effects on the maintenance of these cells due to their quiescent nature. Disclosures No relevant conflicts of interest to declare.
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Ankudinov, A. S., та A. N. Kalyagin. "Сhronic heart failure associated with rheumatoid arthritis: role of inflammation in changing the level of atrial sodium uretic peptide and lipidogram indicators". Siberian Medical Review, № 6 (2020): 64–69. http://dx.doi.org/10.20333/2500136-2020-6-64-69.
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The aim of the research is the analysis of basic clinical laboratory and instrumental parameters of patients suffering from CHF with intermediate left ventricular ejection fraction (LEF), developed as a result of ischemic heart disease and arterial hypertension associated with RA compared to patients without RA; assessment of indicators of morphological and functional parameters of myocardium and possible associations with indicators of RA inflammation activity. Material and methods. The study group included 134 patients with HFFV associated with RA; the comparison group was of 122 patients with HFFV without RA. CHF functional class of patients who took part in the study according to NYHA I-II. RA was diagnosed based on X-ray and serological studies, which included determination of rheumatoid factor (RF), antibodies to cyclic citrullinated peptide (ACCP), C - reactive protein (CRP). Inflammatory process activity was assessed by DAS28 index and visual analogue pain scale (VAS). X-ray RA stage included the studied I-III patients according to Steinbrocker classofication. CHF treatment medications were compared in groups. The basic anti-inflammatory medication for RA treatment is methotrexate. Patients who did not take methotrexate due to side effects and / or individual intolerance took leflunomide at a dosage of 20 mg per day. Moreover, NSAIDs were used (enterally, parenterally, locally). Hematological, biochemical and instrumental studies were carried out. The processing was carried out in STATISTICA 10.0 program. The work presents statistically significant results. The critical level of significance when testing statistical hypotheses is p <0.05. Results. Comparative analysis revealed statistically significant differences in the levels of ESR and CRP, with a predominance of values in the study group, which naturally reflects the intensity of inflammatory process. Furthermore, statistically significant differences in the levels of creatinine and GFR were revealed. It can be due to the influence of chronic inflammation and regular intake of NSAIDs. In the group of patients with CHF on the background of RA, statistically significant decrease in hemoglobin level was found. Statistically significant predominance of TG, LDL-C concentration, as well as a decrease in HDL-C in the study group in relation to the comparison group were obtained. Statistically significant predominance of atherogenic coefficient was revealed in the study group. NT-proBNP concentration in the study groups differed significante: in the group of patients with CHF associated with RA, the level was 306.7 (225; 391) pg / ml; in the CHF group without RA - 488.7 (355; 638) (p = 0.02). A direct association of the DAS28 index and NT-proBNP was found (r = 0.04; p = 0.02). Conclusion. Patients with CHF associated with RA are reasonably recommended to increase the dosage of statins with more frequent monitoring of lipid profile. An assessment of NT-proBNP level is required for more detailed assessment of morphological and functional parameters of myocardium.
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Bacevich, Andrew J. "Left, Right, Left: Opinion." Historically Speaking 2, no. 3 (2001): 5–7. http://dx.doi.org/10.1353/hsp.2001.0020.
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Lefort, Julie. "On the reflexive-possessive markers in the Dongxiang language." Language and Linguistics / 語言暨語言學 21, no. 4 (2020): 581–600. http://dx.doi.org/10.1075/lali.00071.lef.
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Abstract Dongxiang is a language mainly spoken in the Autonomous District of southwest Gansu Province, People’s Republic of China. The Dongxiang nationality (東鄉族), as they are officially called, represents about 300,000 speakers. The Dongxiang language is one of the peripheral Mongolic languages spoken in the Gansu-Qinghai area, also known as the Shirongol group. These languages have been isolated from the other Mongolic languages and have been influenced by the surrounding Chinese dialects to a greater or lesser degree. They have common typological forms inherited from Middle Mongolian as well as features which have been induced by language contact. In this paper, I shall discuss the reflexive possessive markers in the Dongxiang language with a special focus on the suffix -nugvun. I shall show that the functions and use of Dongxiang reflexive possessive markers -ni and -ne are similar to those of the common Mongolic markers *-ni and *-xAn. The reflexive possessive marker -nugvun seems to be found in Dongxiang only and its origin remains unclear. In sources available from the 1980s to the 2000s, it is found associated with a restrictive number of pronouns, nouns, and idiomatic expressions and is highly grammaticalized. However, in more recent sources, it is found associated with a greater number of nouns and seems to have more semantic implications. Moreover, it is also found in a role which could be associated with that of a pronoun, and which can receive a plural and reflexive morphology. Nugvun can be used completely independently and is probably a calque of the Chinese dialect of Linxia 個家ge42 jia243 . This shows that it is most probably an innovation developed from the original suffix.
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Amry, Nelly. "Le samā‘ dans les milieux soufis du Maghreb (VIIe-Xe/XIIIe-XVIe siècles) : pratiques, tensions et codification." Al-Qanṭara 30, no. 2 (2009): 491–528. http://dx.doi.org/10.3989/alqantara.2009.v30.i2.88.
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Morrison, Hope. "Leaf (review)." Bulletin of the Center for Children's Books 62, no. 10 (2009): 405–6. http://dx.doi.org/10.1353/bcc.0.0957.
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Ben Mrad, Ibrahim. "Les gloses botaniques andalouses sur le manuscrit de Paris de la traduction arabe de la Materia Medica de Dioscorides." Al-Qanṭara 30, no. 2 (2009): 581–622. http://dx.doi.org/10.3989/alqantara.2009.v30.i2.91.
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Goločorbin-Kon, Svetlana, Aleksandra Mikov, Velibor Vasović, et al. "Botulinum toxin: Poison and medicine." PONS - medicinski casopis 16, no. 1 (2019): 24–31. http://dx.doi.org/10.5937/pomc16-19715.
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