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Journal articles on the topic 'ThBr4'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Brown, R. J. C., A. Christides, M. Gourdji, and L. Guibé. "NQR investigation on ThBr4 and instrumentation." Journal of Molecular Structure 192, no. 3-4 (January 1989): 355–67. http://dx.doi.org/10.1016/0022-2860(89)85055-0.

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2

Simoni, E., S. Hubert, and M. Genet. "Optical properties of U4+ in α-ThBr4." Inorganica Chimica Acta 139, no. 1-2 (December 1987): 269–71. http://dx.doi.org/10.1016/s0020-1693(00)84092-x.

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3

Simoni, E., S. Hubert, and M. Genet. "Intrinsic photoluminescence of pure β-ThBr4 single crystal." Journal of Luminescence 62, no. 3-4 (October 1994): 139–45. http://dx.doi.org/10.1016/0022-2313(94)90340-9.

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4

Zwanenburg, G., C. P. Keijzers, E. de Boer, and J. C. Krupa. "EPR-study of ThBr4:Pa4+ in the incommensurable phase." Journal of Molecular Structure 173 (January 1988): 397–404. http://dx.doi.org/10.1016/0022-2860(88)80071-1.

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5

Hubert, Solange, and Eric Simoni. "Luminescence and photoconductivity of pure β-ThBr4 single crystal." Journal of Luminescence 40-41 (February 1988): 349–50. http://dx.doi.org/10.1016/0022-2313(88)90227-x.

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6

Hubert, Solange, Chong Li Song, Michel Genet, and François Auzel. "Up conversion process in U4+-doped ThBr4 and ThCl4." Journal of Solid State Chemistry 61, no. 2 (February 1986): 252–59. http://dx.doi.org/10.1016/0022-4596(86)90029-0.

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7

Keijzers, C. P., G. Zwanenburg, J. M. Vervuurt, E. de Boer, and J. C. Krupa. "Single-crystal EPR investigation of the incommensurate phase of ThBr4:Pa4+." Journal of Physics C: Solid State Physics 21, no. 4 (February 10, 1988): 659–67. http://dx.doi.org/10.1088/0022-3719/21/4/004.

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8

Deubner, H. Lars, Stefan Sebastian Rudel, and Florian Kraus. "A Simple Access to Pure Thorium(IV) Halides (ThCl4, ThBr4, and ThI4)." Zeitschrift für anorganische und allgemeine Chemie 643, no. 23 (October 23, 2017): 2005–10. http://dx.doi.org/10.1002/zaac.201700356.

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9

Hubert, S., J. Emery, N. Edelstein, and J. C. Fayet. "Electron paramagnetic resonance of Gd3+ in ThBr4 single crystals at room temperature." Solid State Communications 54, no. 12 (June 1985): 1085–90. http://dx.doi.org/10.1016/0038-1098(85)90766-5.

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10

Cohen, Y., and J. Emery. "E. P. R. evidency of fluctuations near critical temperature in incommensurate ThBr4: Gd3+." Ferroelectrics 125, no. 1 (January 1992): 431–36. http://dx.doi.org/10.1080/00150199208017106.

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11

Cohen, Y., J. Emery, G. Silly, and S. Hubert. "Particular behaviour of the EPR Gd3+probe in the incommensurate phase of ThBr4." Journal of Physics: Condensed Matter 7, no. 21 (May 22, 1995): 4001–17. http://dx.doi.org/10.1088/0953-8984/7/21/002.

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12

Briat, B., P. Delamoye, J. C. Rivoal, S. Hubert, and P. Evesque. "Spectroscopic study of the incommensurate phase of ThBr4 via the optical and magnetooptical properties of U4+." Journal de Physique 46, no. 8 (1985): 1375–86. http://dx.doi.org/10.1051/jphys:019850046080137500.

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13

Chen, Songhua, and David C. Ailion. "Br79nuclear-quadrupole-resonance line shape and Raman-induced spin-lattice relaxation in the incommensurate phase ofβ-ThBr4." Physical Review B 40, no. 4 (August 1, 1989): 2332–40. http://dx.doi.org/10.1103/physrevb.40.2332.

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14

Madariaga, G., J. M. Pérez-Mato, and I. Aramburu. "Phasons modulate the atomic Debye–Waller factors in incommensurate structures: experimental evidence in ThBr4 at 55 K." Acta Crystallographica Section B Structural Science 49, no. 2 (April 1, 1993): 244–54. http://dx.doi.org/10.1107/s0108768192010103.

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15

Hubert, S., E. Simoni, and M. Genet. "Stark energy level determination of the 3H4 ground state of U4+ in the low temperature form α-ThBr4." Journal of the Less Common Metals 122 (August 1986): 81–88. http://dx.doi.org/10.1016/0022-5088(86)90396-6.

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16

Ghag, Snehal, and Suresh Pawar. "Extraction and separation of U(VI) and Th(IV) from hydrobromic acid media using Cyanex-923 extractant." Journal of the Serbian Chemical Society 75, no. 11 (2010): 1549–57. http://dx.doi.org/10.2298/jsc090617118g.

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A systematic study of the solvent extraction of uranium(VI) and thorium(IV) from hydrobromic acid media was performed using the neutral phosphine oxide extractant Cyanex-923 in toluene. These metal ions were found to be quantitatively extracted with Cyanex-923 in toluene in the acidity range 5x10-5-1x10-4 M and 5x10-5-5x10-3 M, respectively, and they are stripped from the organic phase with 7.0 M HClO4 and 2.0- 4.0 M HCl, respectively. The effect of the equilibrium period, diluents, diverse ions and stripping agent on the extraction of U(VI) and Th(IV) was studied. The stoichiometry of the extracted species of these metal ions was determined based on the slope analysis method. The extraction reactions proceed by solvation and their probable extracted species found in the organic phase were UO2Br2?2Cyanex-923 and ThBr4?2Cyanex-923. Based on these results, a sequential procedure for their separation from each other was developed.

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17

Beeching, L. J., J. M. Dyke, A. Morris, and J. S. Ogden. "Study of the electronic structure of the actinide tetrabromides ThBr4 and UBr4 using ultraviolet photoelectron spectroscopy and density functional calculations." Journal of Chemical Physics 114, no. 22 (June 8, 2001): 9832–39. http://dx.doi.org/10.1063/1.1370945.

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18

Clark, David L., Tracey M. Frankcom, Mary M. Miller, and John G. Watkin. "Facile solution routes to hydrocarbon-soluble Lewis base adducts of thorium tetrahalides. Synthesis, characterization, and x-ray structure of ThBr4(THF)4." Inorganic Chemistry 31, no. 9 (April 1992): 1628–33. http://dx.doi.org/10.1021/ic00035a021.

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19

Emery, J., S. Hubert, and J. C. Fayet. "Influence of the coupling in quadrature of two displacement modes and of the phase of the modulation wave on e.s.r. line shapes and relaxation, in the incommensurate phase of ThBr4 : Gd3+." Journal de Physique 46, no. 12 (1985): 2099–105. http://dx.doi.org/10.1051/jphys:0198500460120209900.

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20

Kim, Min Seob, Hyun Seok Choi, Moxin Wu, JiYeon Myung, Eui Joong Kim, Yong Sung Kim, Seungil Ro, et al. "Potential Role of PDGFRβ-Associated THBS4 in Colorectal Cancer Development." Cancers 12, no. 9 (September 6, 2020): 2533. http://dx.doi.org/10.3390/cancers12092533.

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Colorectal cancer is a significant cause of death since it frequently metastasizes to several organs such as the lung or liver. Tumor development is affected by various factors, including a tumor microenvironment, which may be an essential factor that leads to tumor growth, proliferation, invasion, and metastasis. In the tumor microenvironment, abnormal changes in various growth factors, enzymes, and cytokines can wield a strong influence on cancer. Thrombospondin-4 (THBS4), which is an extracellular matrix protein, also plays essential roles in the tumor microenvironment and mediates angiogenesis by transforming growth factor-β (TGFβ) signaling. Platelet-derived growth factor receptor β (PDGFRβ), which is a receptor tyrosine kinase and is also a downstream signal of TGFβ, is associated with invasion and metastasis in colorectal cancer. We identified that PDGFRβ and THBS4 are overexpressed in tumor tissues of colorectal cancer patients, and that PDGF-D expression increased after TGFβ treatment in the colon cancer cell line DLD-1. TGFβ and PDGF-D increased cellular THBS4 protein levels and secretion but did not increase THBS4 mRNA levels. This response was further confirmed by the inositol 1,4,5-triphosphate receptor (IP3R) and stromal interaction molecule 1 (STIM1) blockade as well as the PDGFRβ blockade. We propose that the PDGFRβ signal leads to a modification of the incomplete form of THBS4 to its complete form through IP3R, STIM1, and Ca2+-signal proteins, which further induces THBS4 secretion. Additionally, we identified that DLD-1 cell-conditioned medium stimulated with PDGF-D promotes adhesion, migration, and proliferation of colon myofibroblast CCD-18co cells, and this effect was intensified in the presence of thrombin. These findings suggest that excessive PDGFRβ signaling due to increased TGFβ and PDGF-D in colorectal tumors leads to over-secretion of THBS4 and proliferative tumor development.

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21

Nemec, Corey M., Fan Yang, Joshua M. Gilmore, Corinna Hintermair, Yi-Hsuan Ho, Sandra C. Tseng, Martin Heidemann, et al. "Different phosphoisoforms of RNA polymerase II engage the Rtt103 termination factor in a structurally analogous manner." Proceedings of the National Academy of Sciences 114, no. 20 (May 2, 2017): E3944—E3953. http://dx.doi.org/10.1073/pnas.1700128114.

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The carboxyl-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) orchestrates dynamic recruitment of specific cellular machines during different stages of transcription. Signature phosphorylation patterns of Y1S2P3T4S5P6S7 heptapeptide repeats of the CTD engage specific “readers.” Whereas phospho-Ser5 and phospho-Ser2 marks are ubiquitous, phospho-Thr4 is reported to only impact specific genes. Here, we identify a role for phospho-Thr4 in transcription termination at noncoding small nucleolar RNA (snoRNA) genes. Quantitative proteomics reveals an interactome of known readers as well as protein complexes that were not known to rely on Thr4 for association with Pol II. The data indicate a key role for Thr4 in engaging the machinery used for transcription elongation and termination. We focus on Rtt103, a protein that binds phospho-Ser2 and phospho-Thr4 marks and facilitates transcription termination at protein-coding genes. To elucidate how Rtt103 engages two distinct CTD modifications that are differentially enriched at noncoding genes, we relied on NMR analysis of Rtt103 in complex with phospho-Thr4– or phospho-Ser2–bearing CTD peptides. The structural data reveal that Rtt103 interacts with phospho-Thr4 in a manner analogous to its interaction with phospho-Ser2–modified CTD. The same set of hydrogen bonds involving either the oxygen on phospho-Thr4 and the hydroxyl on Ser2, or the phosphate on Ser2 and the Thr4 hydroxyl, can be formed by rotation of an arginine side chain, leaving the intermolecular interface otherwise unperturbed. This economy of design enables Rtt103 to engage Pol II at distinct sets of genes with differentially enriched CTD marks.

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22

Palao, Teresa, Catarina Rippe, Henk van Veen, Ed VanBavel, Karl Swärd, and Erik N. T. P. Bakker. "Thrombospondin-4 knockout in hypertension protects small-artery endothelial function but induces aortic aneurysms." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (June 1, 2016): H1486—H1493. http://dx.doi.org/10.1152/ajpheart.00046.2016.

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Thrombospondin-4 (TSP-4) is a multidomain calcium-binding protein that has both intracellular and extracellular functions. As an extracellular matrix protein, it is involved in remodeling processes. Previous work showed that, in the cardiovascular system, TSP-4 expression is induced in the heart in response to experimental pressure overload and infarction injury. Intracellularly, it mediates the endoplasmic reticulum stress response in the heart. In this study, we explored the role of TSP-4 in hypertension. For this purpose, wild-type and TSP-4 knockout ( Thbs4 −/−) mice were treated with angiotensin II (ANG II). Hearts from ANG II-treated Thbs4 −/− mice showed an exaggerated hypertrophic response. Interestingly, aortas from Thbs4 −/− mice treated with ANG II showed a high incidence of aneurysms. In resistance arteries, ANG II-treated wild-type mice showed impaired endothelial-dependent relaxation. This was not observed in ANG II-treated Thbs4 −/− mice or in untreated controls. No differences were found in the passive pressure-diameter curves or stress-strain relationships, although ANG II-treated Thbs4 −/− mice showed a tendency to be less stiff, associated with thicker diameters of the collagen fibers as revealed by electron microscopy. We conclude that TSP-4 plays a role in hypertension, affecting cardiac hypertrophy, aortic aneurysm formation, as well as endothelial-dependent relaxation in resistance arteries.

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23

Procházka, Zdenko, Jiřina Slaninová, Tomislav Barth, Alena Stierandová, Jerzy Trojnar, Per Melin, and Michal Lebl. "Analogs of Deamino Carba Oxytocin with Inhibitory Properties; Synthesis and Biological Activities." Collection of Czechoslovak Chemical Communications 57, no. 6 (1992): 1335–44. http://dx.doi.org/10.1135/cccc19921335.

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Solid phase methodology on polyamide-kieselguhr resin was used for the synthesis of six analogs of deamino carba-1 or carba-6 oxytocin with non-coded amino acids in position 2, threonine in position 4, ornithine in position 8 and without glycine in position 9. The following analogs were prepared: des-Gly9-[L-Phe(p-Et)2, Thr4, Orn8]deamino-carba-1-oxytocin (I), des-Gly9-[D-Phe(p-Et)2, Thr4, Orn8]deamino-carba-1-oxytocin (II), des-Gly9-[D-Tyr(Et)2, Thr4, Orn8]deamino-carba-1-oxytocin (III), des-Gly9-[L-Phe(p-Et)2, Thr4, Orn8]deamino-carba-6-oxytocin (IV), des-Gly9-[D-Phe(p-Et)2, Thr4, Orn8]deamino-carba-6-oxytocin (V), and des-Gly9-[D-Tyr(Et)2, Thr4, Orn8]deamino-carba-1-oxytocin (VI). All the analogs were found to be strong uterotonic and pressor inhibitors. The highest potency in the uterotonic inhibitory test was exhibited by analog II (pA2 = 8.3) and strongest pressor inhibitor was compound I (pA2 = 7.5).

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24

Cantau, B., J. N. Barjon, D. Chicot, P. P. Baskevitch, and S. Jard. "Oxytocin receptors from LLC-PK1 cells: expression in Xenopus oocytes." American Journal of Physiology-Renal Physiology 258, no. 4 (April 1, 1990): F963—F972. http://dx.doi.org/10.1152/ajprenal.1990.258.4.f963.

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Two selective radioligands for oxytocin receptors, [3H]-[4-threonine,7-glycine]oxytocin [( 3H]-[Thr4,Gly7]OT) and 125I-[1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine, 4-threonine, 8-ornithine, 9-tyrosine amide]-oxytocin (125I-OTA), were used to characterize oxytocin receptors from two pig kidney-derived cell lines, LLC-PK1 and LLC-PK1L. [3H]-[Thr4,Gly7]OT and 125I-OTA bind with high affinity (mean Kd values of 14 and 0.06 nM, respectively) to the same population of sites on LLC-PK1 cell membranes [maximum binding (Bmax) of 100 fmol/mg membrane protein]. These sites had the expected ligand selectivity of oxytocin receptors. [3H]-[Thr4,Gly7]OT and 125I-OTA binding sites could be distinguished from V2 vasopressin receptors present on LLC-PK1 and LLC-PK1L cells on the basis of clearly different maximal capacities and ligand selectivities, different sensitivities to insulin and serum, and absence of heterologous downregulation. Oxytocin receptors from LLC-PK1 cells have no functional relationship with adenylate cyclase. [Thr4,Gly7]OT affected neither the basal adenosine 3',5'-cyclic monophosphate (cAMP) content nor the vasopressin-induced cAMP accumulation by LLC-PK1 cells. Xenopus laevis oocytes injected with LLC-PK1 cell mRNA responded to [Thr4,Gly7]OT by an increase in 45Ca2+ outflux; this effect is antagonized by a highly selective oxytocin antagonist.

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25

Gan, Kathlyn J., and Thomas C. Südhof. "Specific factors in blood from young but not old mice directly promote synapse formation and NMDA-receptor recruitment." Proceedings of the National Academy of Sciences 116, no. 25 (June 3, 2019): 12524–33. http://dx.doi.org/10.1073/pnas.1902672116.

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Aging drives a progressive decline in cognition and decreases synapse numbers and synaptic function in the brain, thereby increasing the risk for neurodegenerative disease. Pioneering studies showed that introduction of blood from young mice into aged mice reversed age-associated cognitive impairments and increased synaptic connectivity in brain, suggesting that young blood contains specific factors that remediate age-associated decreases in brain function. However, whether such factors in blood from young animals act directly on neurons to enhance synaptic connectivity, or whether they act by an indirect mechanism remains unknown. Moreover, which factors in young blood mediate cognitive improvements in old mice is incompletely understood. Here, we show that serum extracted from the blood of young but not old mice, when applied to neurons transdifferentiated from human embryonic stem cells, directly increased dendritic arborization, augmented synapse numbers, doubled dendritic spine-like structures, and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasing synaptic connectivity. Mass spectrometry revealed that thrombospondin-4 (THBS4) and SPARC-like protein 1 (SPARCL1) were enriched in serum from young mice. Strikingly, recombinant THBS4 and SPARCL1 both increased dendritic arborization and doubled synapse numbers in cultured neurons. In addition, SPARCL1 but not THBS4 tripled NMDA receptor-mediated synaptic responses. Thus, at least two proteins enriched in young blood, THBS4 and SPARCL1, directly act on neurons as synaptogenic factors. These proteins may represent rejuvenation factors that enhance synaptic connectivity by increasing dendritic arborization, synapse formation, and synaptic transmission.

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26

Liu, Jinliang, Gong Cheng, Haiwei Yang, Xiaheng Deng, Chao Qin, Lixin Hua, and Changjun Yin. "Reciprocal regulation of long noncoding RNAs THBS4-003 and THBS4 control migration and invasion in prostate cancer cell lines." Molecular Medicine Reports 14, no. 2 (June 23, 2016): 1451–58. http://dx.doi.org/10.3892/mmr.2016.5443.

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27

Windle, R. J., J. M. Judah, and M. L. Forsling. "Effect of oxytocin receptor antagonists on the renal actions of oxytocin and vasopressin in the rat." Journal of Endocrinology 152, no. 2 (February 1997): 257–64. http://dx.doi.org/10.1677/joe.0.1520257.

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Abstract The effect of three oxytocin receptor antagonists on the renal actions of oxytocin and vasopressin was investigated in conscious male rats infused with hypotonic saline. Infusion of oxytocin at 100 pg/min produced plasma concentrations of 12·7 ± 3·3 pmol/l and led to significant increases in sodium excretion, urine flow and glomerular filtration rate (GFR). The increase in sodium excretion of 42 ± 9% during oxytocin infusion was significantly decreased by all three antagonists to 15 ± 5% (10 ng [mercapto-proprionic acid1,d-Tyr(Et)2, Thr4,Orn8]-oxytocin/min), 13 ± 5% (5 ng desGly9[d-Trp2,Thr4,Orn8]-dC6oxytocin/min) and 4 ± 5% (1 ng d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr(NH2)9]-vasotocin/min). Similarly, the increase in urine production of 22 ± 5% associated with oxytocin infusion was significantly decreased to 4 ± 3% (5 ng desGly9[d-Trp2,d-Thr4,Orn8]-dC6oxytocin/min) and 1 ± 4% (1 ng d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr(NH2)9]-vasotocin/min). All three antagonists blocked the oxytocin-induced increase in GFR when infused at 10 ng/min. Infusion of vasopressin at 160 pg/min produced plasma concentrations of 10·1 ± 2·1 pmol/l and this led to a significant increase in sodium excretion and a significant decrease in urine flow rate. None of the antagonists had any effect on the natriuretic or antidiuretic actions of vasopressin suggesting that different receptors are involved in these renal actions of the two peptides. Journal of Endocrinology (1997) 152, 257–264

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28

Ammar, A., S. Roseau, and D. Butlen. "Pharmacological characterization of V1a vasopressin receptors in the rat cortical collecting duct." American Journal of Physiology-Renal Physiology 262, no. 4 (April 1, 1992): F546—F553. http://dx.doi.org/10.1152/ajprenal.1992.262.4.f546.

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Vasopressin receptors in distal segments of the rat nephron were identified in isolated tubules using two labeled ligands: the [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine,4-threonine,8-ornithine,9-125I-tyrosylamide]- vasotocin [125I-d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT] and the linear analogue, Phaa1,D-Tyr(Me)2,Phe3,Gln4,Asn5,Arg6, Pro7,Arg8,125I-Tyr-NH2(9) [125I-Tyr-NH2(9)-linear antagonist (LA)-V1a)]. Specific 125I-d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]-OVT binding to cortical collecting ducts (CCD) was saturable with incubation time and dose, reversible after elimination of free ligand, and characterized by the following rank order for recognition of vasopressin analogues: desGly9-d-(CH2)5-[Tyr(Et)2,Val4]arginine vasopressin (AVP) greater than or equal to d(CH2)5[Tyr-(ET)2,Val4]AVP greater than or equal to AVP greater than or equal to d(CH2)5[Tyr(Me)2]AVP = 1-desamino-8-D-arginine vasopressin (DDAVP) greater than or equal to Tyr-NH2(9)-LA-V1a greater than [8-arginine]vasotocin (AVT) greater than d(CH2)5[Tyr(Me)2, Thr4,Tyr-NH2(9)]OVT greater than oxytocin (OT) greater than [Phe2,Orn8]VT much greater than [Thr4,Gly7]-OT. Scatchard plots of dose-dependent 125I-Tyr-NH2(9)-LA-V1a binding to medullary thick ascending limbs (MTAL), CCD, and outer medullary collecting ducts (OMCD) revealed the presence of high- and low-affinity binding sites corresponding to V1a and V2 vasopressin receptors, respectively; the densities of V1a receptors are approximately 20% of the total number of vasopressin receptors in CCD and 5% in MTAL and OMCD.

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29

Reidelberger, R. D., T. J. Kalogeris, and T. E. Solomon. "Plasma CCK levels after food intake and infusion of CCK analogues that inhibit feeding in dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 5 (May 1, 1989): R1148—R1154. http://dx.doi.org/10.1152/ajpregu.1989.256.5.r1148.

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To determine whether postprandial plasma levels of cholecystokinin (CCK) are sufficient to produce satiety, we compared CCK levels after food intake and administration of CCK analogues that suppress feeding. Seven beagles were adapted to ad libitum access to solid food for 18 h, which was followed by 4 h of food deprivation and a 1-h test session. Plasma CCK increased from 2.7 +/- 0.2 pM before to a maximum of 5.0 +/- 0.7 pM after ingestion of solid food. Intravenous cholecystokinin octapeptide (CCK-8; 0, 50, 100, 200, 400, 800 pmol.kg-1.h-1), caerulein (0, 25, 50, 100, 200, 400 pmol.kg-1.h-1), and [Thr4,Nle7]CCK-9 (0, 25, 50, 100, 200, 400 pmol.kg-1.h-1), at a rate of 1 dose/day given 15 min before feeding and during a 45-min feeding period, caused similar dose-dependent suppression of feeding at 200 pmol.kg-1.h-1 and greater. On separate days blood samples for peptide assay were collected during infusion of scalar ascending doses of CCK-8 or [Thr4,Nle7]CCK-9 (0, 25, 50, 100, 200, 400 pmol.kg-1.h-1) or caerulein (0, 16.7, 50, and 150 pmol.kg-1.h-1), with each dose being administered for 30 min. Peptide levels were highly correlated with dose (r = 0.94, 0.87, and 0.95 for CCK-8, caerulein, and [Thr4,Nle7]CCK-9, respectively). Peptide levels after minimal effective doses for suppression of feeding were 59 +/- 6, 54 +/- 7, and 70 +/- 5 pM for CCK-8, caerulein, and [Thr4,Nle7]CCK-9. These results suggest that postprandial plasma levels of CCK are not sufficient to produce satiety.

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30

Ma, Lina, Xinghui Sun, Yurong Li, and Na Liu. "Identification of Bioinformatics of the Metastasis of Endometrial Carcinoma Based on Gene Expression Microarray." Journal of Biomaterials and Tissue Engineering 10, no. 6 (June 1, 2020): 776–81. http://dx.doi.org/10.1166/jbt.2020.2330.

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Objective: We aimed to explore the bioinformatics of endometrial carcinoma (EC) metastasis. Methods: The microarray information of 4 cases of progressive endometrial cancer (PEC) and 4 cases of non-progressive controls (NPC) were collected from the Gene Expression Omnibus Database (GEOD). The Limma package in R was performed to selected the differentially expressed genes (DEGs). Then, the hierarchical clustering of DEGs was carried out. In addition, bioinformatics analysis was carried out. Results: There were 65 DEGs identified between PEC and NPC. Those DEGs were mostly enriched in cell proliferation function, MAPK and TGF-β signaling pathways. Furthermore, those DEGs were related to of the increased contents of IGF2 and PLAG1, and decreased contents of THBS4 and FGF20. Conclusions: There were 65 DEGs identified in endometrial cancer between progressive and non-progressive. Those DEGs were significantly related to tumor metastasis. Increased levels of IGF2 and PLAG1, and decreased levels of THBS4 and FGF20 may have a notable effect on the development of EC.

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31

Mayer, Andreas, Martin Heidemann, Michael Lidschreiber, Amelie Schreieck, Mai Sun, Corinna Hintermair, Elisabeth Kremmer, Dirk Eick, and Patrick Cramer. "CTD Tyrosine Phosphorylation Impairs Termination Factor Recruitment to RNA Polymerase II." Science 336, no. 6089 (June 28, 2012): 1723–25. http://dx.doi.org/10.1126/science.1219651.

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In different phases of the transcription cycle, RNA polymerase (Pol) II recruits various factors via its C-terminal domain (CTD), which consists of conserved heptapeptide repeats with the sequence Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7. We show that the CTD of transcribing yeast Pol II is phosphorylated at Tyr1, in addition to Ser2, Thr4, Ser5, and Ser7. Tyr1 phosphorylation stimulates binding of elongation factor Spt6 and impairs recruitment of termination factors Nrd1, Pcf11, and Rtt103. Tyr1 phosphorylation levels rise downstream of the transcription start site and decrease before the polyadenylation site, largely excluding termination factors from gene bodies. These results show that CTD modifications trigger and block factor recruitment and lead to an extended CTD code that explains transcription cycle coordination on the basis of differential phosphorylation of Tyr1, Ser2, and Ser5.

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Zwanenburg, G., C. P. Keijzers, E. De Boer, and J. C. Krupa. "Simulation of EPR spectra of ThBr8:Pa4+ in the incommensurable phase." Chemical Physics Letters 140, no. 1 (September 1987): 11–14. http://dx.doi.org/10.1016/0009-2614(87)80407-4.

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Sanchez, Ana M., Stewart Shuman, and Beate Schwer. "RNA polymerase II CTD interactome with 3′ processing and termination factors in fission yeast and its impact on phosphate homeostasis." Proceedings of the National Academy of Sciences 115, no. 45 (October 24, 2018): E10652—E10661. http://dx.doi.org/10.1073/pnas.1810711115.

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The carboxy-terminal domain (CTD) code encrypted within the Y1S2P3T4S5P6S7heptad repeats of RNA polymerase II (Pol2) is deeply rooted in eukaryal biology. Key steps to deciphering the code are identifying the events in gene expression that are governed by individual “letters” and then defining a vocabulary of multiletter “words” and their meaning. Thr4 and Ser7 exert opposite effects on the fission yeastpho1gene, expression of which is repressed under phosphate-replete conditions by transcription of an upstream flanking long noncoding RNA (lncRNA). Here we attribute the derepression ofpho1by a CTD-S7Amutation to precocious termination of lncRNA synthesis, an effect that is erased by mutations of cleavage-polyadenylation factor (CPF) subunits Ctf1, Ssu72, Ppn1, Swd22, and Dis2 and termination factor Rhn1. By contrast, a CTD-T4Amutation hyperrepressespho1, as do CPF subunit and Rhn1 mutations, implying thatT4Areduces lncRNA termination. Moreover, CTD-T4Ais synthetically lethal withppn1∆ andswd22∆, signifying that Thr4 and the Ppn1•Swd22 module play important, functionally redundant roles in promoting Pol2 termination. We find that Ppn1 and Swd22 become essential for viability when the CTD array is curtailed and thatS7Aovercomes the need for Ppn1•Swd22 in the short CTD context. Mutational synergies highlight redundant essential functions of (i) Ppn1•Swd22 and Rhn1, (ii) Ppn1•Swd22 and Ctf1, and (iii) Ssu72 and Dis2 phosphatases. CTD allelesY1F,S2A, andT4Ahave overlapping synthetic lethalities withppn1∆ andswd22∆, suggesting that Tyr1-Ser2-Thr4 form a three-letter CTD word that abets termination, with Rhn1 being a likely “reader” of this word.

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Ammar, A., R. M. Rajerison, S. Roseau, M. Bloch-Faure, and D. Butlen. "Frog glomerular vasotocin receptors resemble mammalian V1b receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 5 (November 1, 1994): R1198—R1208. http://dx.doi.org/10.1152/ajpregu.1994.267.5.r1198.

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Vasotocin receptors were investigated in glomeruli and nephron segments microdissected from collagenase-treated kidneys of Rana ridibunda, using [d(CH2)5Tyr(Me)2,Thr4,Orn8,125I-Tyr-NH2(9)]vasotocin (125I-OVTA) as a radioligand. Specific 125I-OVTA binding sites were found only in glomeruli and not in all tubule segments tested. Glomerular receptors exhibited the following stereospecificity for recognition of vasotocin analogues: Tyr-NH2(9)-LA-V1a > 125I-OVTA > arginine vasotocin (AVT) > or = [d(CH2)5Tyr-(Me)2]AVP > OVTA > or = [Phe2,Orn8]VT > oxytocin (OT) > or = [d(CH2)5-Sar7]AVP > desGly9[d(CH2)5Tyr(Et)2]VAVP > or = [d(CH2)5Tyr(Et)2]VAVP > AVP > [1-desamino-8-D-arginine]vasopressin (DDAVP) > [Thr4,Gly7]OT. In addition, vasotocin enhanced [3H]inositol phosphate production in sieved glomeruli labeled with myo-[3H]inositol; the rank order of structural vasotocin analogues for stimulation of phosphoinositidase C was [Phe2,Orn8]VT > AVT > OT > AVP > DDAVP, whereas [Thr4,Gly7]OT was almost inactive, and the rank order of antagonists for inhibition of hormone-induced enzyme activation was Tyr-NH2(9)-LA-V1a > [d(CH2)5Tyr(Me)2]AVP = OVTA > [d(CH2)5Sar7]AVP > [d(CH2)5Tyr(Et)2]VAVP > or = desGly9[d(CH2)5Tyr(Et)2]VAVP. Results indicate that the 125I-OVTA-labeled binding sites detected in frog glomeruli reveal the pharmacological properties of mammalian V1b-pituitary vasopressin receptors and might be physiological vasotocin receptors involved in phosphoinositidase C stimulation.

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35

McLeod, Damian, Gibbe Parsons, Robert Gunther, Anthony Quail, David Cottee, and Saxon White. "Differential effects of inhaled methacholine on circumferential wall and vascular smooth muscle of third-generation airways in awake sheep." Journal of Applied Physiology 113, no. 8 (October 15, 2012): 1233–42. http://dx.doi.org/10.1152/japplphysiol.00133.2012.

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Evolution and natural selection ensure that specific mechanisms exist for selective airway absorption of inhaled atmospheric molecules. Indeed, nebulized cholinoceptor agonists used in asthma-challenge tests may or may not enter the systemic circulation. We examined the hypothesis that inhaled cholinoceptor agonists have selective access. Six sheep were instrumented under general anesthesia (propofol 5 mg/kg iv, 2-3% isoflurane–oxygen), each with pulsed-Doppler blood flow transducers mounted on the single bronchial artery and sonomicrometer probes mounted on the intrapulmonary third-generation lingula lobe bronchus. Continuous measurements were made of bronchial blood flow (Qbr), Qbr conductance (Cbr), bronchial hemicircumference (CIRCbr), and bronchial wall thickness (WALL THbr) in recovered, standing, awake sheep. Methacholine (MCh; 0.125–2.0 μg/kg iv), at the highest dose, caused a 233% rise in Qbr ( P < 0.05) and a 286% rise in Cbr ( P < 0.05). CIRCbr fell to 90% ( P < 0.05); WALL THbr did not change. In contrast, nebulized MCh (1–32 mg/ml), inhaled through a mask at the highest dose, caused a rise in ventilation and a rise in Qbr proportional to aortic pressure without change in Cbr. CIRCbr fell to 91% ( P < 0.01), and WALL THbr did not change. Thus inhaled MCh has access to cholinoceptors of bronchial circumferential smooth muscle to cause airway lumen narrowing but effectively not to those of the systemic bronchovascular circulation. It is speculated that the mechanism is selective neuroparacrine inhibition of muscarinic acetylcholine receptors (M3 bronchovascular cholinoceptors) by prostanoids released by intense MCh activation of epithelial and mucosal cells lining the airway.

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Aas, Sten Freddy, and Sven Erik Rognes. "Nucleotide sequence of the yeast THR4 gene encoding threonine synthase." Nucleic Acids Research 18, no. 3 (1990): 665. http://dx.doi.org/10.1093/nar/18.3.665.

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Guo, Dan, Dan Zhang, Mudan Ren, Guifang Lu, Xu Zhang, Shuixiang He, and Yarui Li. "THBS4 promotes HCC progression by regulating ITGB1 via FAK/PI3K/AKT pathway." FASEB Journal 34, no. 8 (June 22, 2020): 10668–81. http://dx.doi.org/10.1096/fj.202000043r.

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Chen, Xiangbo, Yisen Huang, Yubin Wang, Qiuli Wu, Shunzhong Hong, and Zicheng Huang. "THBS4 predicts poor outcomes and promotes proliferation and metastasis in gastric cancer." Journal of Physiology and Biochemistry 75, no. 1 (February 2019): 117–23. http://dx.doi.org/10.1007/s13105-019-00665-9.

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39

Gonzalez-Iglesias, Arturo E., Patrick A. Fletcher, José A. Arias-Cristancho, Ruth Cristancho-Gordo, Cleyde V. Helena, Richard Bertram, and Joël Tabak. "Direct Stimulatory Effects of Oxytocin in Female Rat Gonadotrophs and Somatotrophs In Vitro: Comparison With Lactotrophs." Endocrinology 156, no. 2 (November 19, 2014): 600–612. http://dx.doi.org/10.1210/en.2014-1543.

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The peptide oxytocin (OT) is secreted by hypothalamic neurons and exerts numerous actions related to reproduction. OT stimulation of prolactin secretion in female rats is important during the estrous cycle, pregnancy, and lactation. Here we report that OT also stimulates transients of intracellular Ca2+ concentration in somatotrophs and gonadotrophs as well as the release of GH and LH in a dose-dependent manner with EC50 values that closely correspond to the ligand affinity of the OT receptor (OTR). Remarkably, the hormone-releasing effect of OT in these two cell types is 2 orders of magnitude more sensitive than that in lactotrophs. The specific OTR agonist [Thr4,Gly7]-oxytocin acutely stimulated the release of LH, GH, and prolactin from female rat pituitary cells in primary culture and increased intracellular Ca2+ concentration in gonadotrophs, somatotrophs, and lactotrophs. In these three cell types, the effects on hormone release and intracellular Ca2+ of both OT and [Thr4,Gly7]oxytocin were abolished by the specific OT receptor antagonist desGly-NH2-d(CH2)5[D-Tyr2,Thr4]OVT but not by the highly selective vasopressin V1a receptor antagonist, d(CH2)5[Tyr(Me)2,Dab5]AVP. Furthermore, 10 nM arginine vasopressin stimulated LH and GH release comparably with a dose of OT that was at least 10 times lower. Finally, the presence of the OTR-like immunoreactivity could be observed in all three cell types. Taken together, these results show that OT directly stimulates gonadotrophs, somatotrophs, and lactotrophs through OT receptors and suggest that OT signaling may serve to coordinate the release of different pituitary hormones during specific physiological conditions.

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40

Ryan, Dan, Arthur Moss, Jeanette McCarthy, Ilan Goldenberg, Wojciech Zareba, Charles Sparks, and James Corsetti. "Thrombospondin-4 polymorphism (A387P) predicts cardiovascular risk in postinfarction patients with high HDL cholesterol and C-reactive protein levels." Thrombosis and Haemostasis 106, no. 12 (2011): 1170–78. http://dx.doi.org/10.1160/th11-03-0206.

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SummaryFew studies are available in human populations investigating involvement of vascular inflammation and oxidative stress-related dysfunctional transformation of high-density lipoprotein (HDL) in establishing cardiovascular disease (CVD) risk. To this end, the current work investigated a subgroup of post-infarction patients at high-risk for recurrent events defined by high levels of HDL cholesterol (HDL-C) and concurrently high levels of C-reactive protein (CRP). Thrombospondin-4 (TSP-4), a matricellular protein of vessel walls associated with inflammation, was investigated in terms of CVD risk using multivariable modelling with a well-characterised functional genetic polymorphism of THBS4 (A387P, rs1866389) along with previously demonstrated risk-related functional genetic polymorphisms of CYBA (C242T, rs4673) and CETP (TaqIB, rs708272), and a set of blood markers. Results revealed risk-association for the gain-of-function P-allele of the THBS4 polymorphism (hazard ratio 2.00, 95% confidence interval 1.10–3.65, p=0.024). Additionally, von Willebrand factor was associated with D-dimer levels in the higher-risk P allele patients suggestive of a connection between endothelial dysfunction and thrombogenesis. In conclusion, TSP-4, a matricellular protein involved in regulating vascular inflammation, plays a role in establishing recurrent coronary risk in postinfarction patients with high levels of HDL-C and CRP. Further studies should focus on additional effects of vascular inflammatory processes on anti-atherogenic functionality of HDL particles.

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Babizhetskyy, Volodymyr, Arndt Simon, and Kurt Hiebl. "Single Crystal Investigation and Physical Properties of the Binary Compound CeB4." Zeitschrift für Naturforschung B 62, no. 7 (July 1, 2007): 896–900. http://dx.doi.org/10.1515/znb-2007-0704.

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Abstract The structure of CeB4 has been determined by single crystal X-ray diffraction. The compound crystallizes in the ThB4 structure type (space group P4/mbm, a = 7.2034(8), c = 4.1006(5) Å; 270 reflections with Fo ≥ 4σ (Fo), R1 = 0.023, wR2 = 0.052). The results of the magnetic and electrical resistivity measurements indicate a strong f-d hybridization of the 4 f electrons of the cerium atom

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42

Benner, Eric J., Dominic Luciano, Rebecca Jo, Khadar Abdi, Patricia Paez-Gonzalez, Huaxin Sheng, David S. Warner, Chunlei Liu, Cagla Eroglu, and Chay T. Kuo. "Protective astrogenesis from the SVZ niche after injury is controlled by Notch modulator Thbs4." Nature 497, no. 7449 (April 24, 2013): 369–73. http://dx.doi.org/10.1038/nature12069.

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43

Adolph, Kenneth W. "The Zebrafish Thrombospondin 3 and 4 Genes ( thbs3 and thbs4 ): cDNA and Protein Structure." DNA Sequence 13, no. 5 (January 2002): 277–85. http://dx.doi.org/10.1080/1042517021000019278.

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44

Lin, Xiandong, Don Hu, Gang Chen, Yi Shi, Hejun Zhang, Xiaojiang Wang, Xiaoyun Guo, et al. "Associations of THBS2 and THBS4 polymorphisms to gastric cancer in a Southeast Chinese population." Cancer Genetics 209, no. 5 (May 2016): 215–22. http://dx.doi.org/10.1016/j.cancergen.2016.04.003.

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45

Ghobadi, Mohadeseh Zarei, Rahman Emamzadeh, and Sayed-Hamidreza Mozhgani. "Deciphering microRNA-mRNA regulatory network in adult T-cell leukemia/lymphoma; the battle between oncogenes and anti-oncogenes." PLOS ONE 16, no. 2 (February 25, 2021): e0247713. http://dx.doi.org/10.1371/journal.pone.0247713.

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Adult T-cell leukemia/lymphoma (ATLL) is virus-caused cancer that originates from the infection by human T-cell leukemia virus type 1. ATLL dysregulates various biological pathways related to the viral infection and cancer progression through the dysexpression of miRNAs and mRNAs. In this study, the potential regulatory subnetworks were constructed aiming to shed light on the pathogenesis mechanism of ATLL. For this purpose, two mRNA and one miRNA expression datasets were firstly downloaded from the GEO database. Next, the differentially expressed genes and miRNAs (DEGs and DE-miRNAs, respectively), as well as differentially co-expressed gene pairs (DCGs), were determined. Afterward, common DEGs and DCGs targeted by experimentally validated DE-miRNAs were explored. The oncogenic and anti-oncogenic miRNA-mRNA regulatory subnetworks were then generated. The expression levels of four genes and two miRNAs were examined in the blood samples by qRT-PCR. The members of three oncogenic/anti-oncogenic subnetworks were generally enriched in immune, virus, and cancer-related pathways. Among them, FZD6, THBS4, SIRT1, CPNE3, miR-142-3p, and miR-451a were further validated by real-time PCR. The significant up-regulation of FZD6, THBS4, and miR-451a as well as down-regulation of CPNE3, SIRT1, and miR-142-3p were found in ATLL samples than normal samples. The identified oncogenic/anti-oncogenic subnetworks are pieces of the pathogenesis puzzle of ATLL. The ultimate winner is probably an oncogenic network that determines the final fate of the disease. The identified genes and miRNAs are proposed as novel prognostic biomarkers for ATLL.

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Simoni, E., S. Hubert, and M. Genet. "Analysis of the absorption and emission spectra of U4+ in α-ThBr 4." Journal de Physique 49, no. 8 (1988): 1425–34. http://dx.doi.org/10.1051/jphys:019880049080142500.

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47

Wei, Lai, Seeun Ha, Brian Jorgensen, Paul J. Park, Rajan Singh, Hannah Zogg, Sandra Poudrier, Moon Young Lee, and Seungil Ro. "Sa1137 AN ADHESIOGENIC ROLE OF THBS4 IN THE DEVELOPMENT OF POSTSURGICAL ABDOMINAL ADHESIONS IN MICE." Gastroenterology 158, no. 6 (May 2020): S—288. http://dx.doi.org/10.1016/s0016-5085(20)31411-6.

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48

Zhao, Tong, Zhifu Wang, Tongming Zhu, Rong Xie, and Jianhong Zhu. "Downregulation of Thbs4 caused by neurogenic niche changes promotes neuronal regeneration after traumatic brain injury." Neurological Research 42, no. 8 (July 20, 2020): 703–11. http://dx.doi.org/10.1080/01616412.2020.1795590.

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49

Han, J. S., Y. Maeda, and M. A. Knepper. "Dual actions of vasopressin and oxytocin in regulation of water permeability in terminal collecting duct." American Journal of Physiology-Renal Physiology 265, no. 1 (July 1, 1993): F26—F34. http://dx.doi.org/10.1152/ajprenal.1993.265.1.f26.

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We conducted studies in isolated perfused terminal inner medullary collecting ducts (IMCD) from rats to investigate the roles of oxytocin and vasopressin in the regulation of osmotic water permeability. Vasopressin and oxytocin were found to have both stimulatory effects (at 0.1 nM) and inhibitory effects (at 10 nM) on osmotic water permeability. Measurements of adenosine 3',5'-cyclic monophosphate (cAMP) production demonstrated that both vasopressin and oxytocin increase cAMP production. Both the selective oxytocin-receptor agonist [Thr4,Gly7]oxytocin (10 nM) and the selective V1b agonist [deamino1,D-3-(pyridyl)Ala2,Arg8]vasopressin (10 nM) inhibited vasopressin-stimulated osmotic water permeability. In contrast, the selective V1a vasopressin-receptor agonist [Phe2,Ile3,Orn8]vasopressin (10 nM) had no effect on vasopressin-stimulated osmotic water permeability. These effects on water permeability correlated with the ability of the agents to transiently increase intracellular free calcium. The oxytocin/vasopressin-receptor antagonist [des-glycinamide9,d(CH2)5(1),O-Me-Tyr2,Thr4,Orn8]vasot ocin, which almost completely blocks vasopressin-induced calcium mobilization, also blocked the ability of 10 nM vasopressin to inhibit osmotic water permeability relative to that found with 0.1 nM vasopressin. We conclude the following. 1) Oxytocin, like vasopressin, has dual effects on osmotic water permeability, increasing it at subnanomolar concentrations and inhibiting it at suprananomolar concentrations. 2) Oxytocin, like vasopressin, can increase cAMP production, perhaps accounting for the increase in water permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

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50

IIDA, Shin-ichiro, Hideyuki TAKEUCHI, Kentaro KATO, Kazuo YAMAMOTO, and Tatsuro IRIMURA. "Order and maximum incorporation of N-acetyl-d-galactosamine into threonine residues of MUC2 core peptide with microsome fraction of human-colon-carcinoma LS174T cells." Biochemical Journal 347, no. 2 (April 10, 2000): 535–42. http://dx.doi.org/10.1042/bj3470535.

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Mucin 2 (MUC2) is the major intestinal mucin. O-glycans are attached to MUC2 in a potentially diverse arrangement, which is crucial for their interaction with endogeneous and exogeneous lectins. In the present report, five oligopeptides [PTTTPITTTT(K), ITTTTTVTPT(K), TVTPTPTPTG(K), PTPTGTQTPT(K) and TQTPTTTPIT(K)] corresponding to portions of the MUC2 tandem repeat domain were synthesized, and incubated with UDP-N-acetyl-D-galactosamine (UDP-GalNAc) and detergent-soluble microsomes, prepared from the human colon carcinoma cell line LS174T. The products were fractionated by reverse-phase HPLC and characterized by matrix-assisted laser-desorption ionization-time-of-flight mass spectrometry. Oligopeptides with GalNAc residues derived from PTTTPITTTT(K), containing consecutive threonine residues, were found to be glycosylated with 1-7 GalNAc residues per single peptide. The sequences of all glycopeptides were determined. The results indicated that the predominant sites of the first through to the sixth GalNAc incorporation were Thr3, Thr6, Thr5, Thr2, Thr4 and Thr1, respectively. An exception was the presence of a glycopeptide with three GalNAc residues at Thr1, Thr4 and Thr5. Oligopeptides containing alternating threonine residues [TVTPTPTPTG(K) and PTPTGTQTPT(K)] were not fully glycosylated under the same conditions or even after prolonged incubations. Thus, the preferential order and maximum number of GalNAc incorporation into threonine residues of MUC2 core peptides depends on the peptide sequence, when the microsome fraction of LS174T cells is used as a source of N-acetyl-D-galactosaminyltransferases.

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