Gotowe bibliografie tematyczne / Sugp1

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Gotowa bibliografia na temat „Sugp1”

Autor: Grafiati

Data publikacji: 15 marca 2025

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Artykuły w czasopismach na temat "Sugp1"

Liu, Zhaoqi, Jian Zhang, Yiwei Sun, Tomin E. Perea-Chamblee, James L. Manley i Raul Rabadan. "Pan-cancer analysis identifies mutations in SUGP1 that recapitulate mutant SF3B1 splicing dysregulation". Proceedings of the National Academy of Sciences 117, nr 19 (24.04.2020): 10305–12. http://dx.doi.org/10.1073/pnas.1922622117.

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The gene encoding the core spliceosomal protein SF3B1 is the most frequently mutated gene encoding a splicing factor in a variety of hematologic malignancies and solid tumors. SF3B1 mutations induce use of cryptic 3′ splice sites (3′ss), and these splicing errors contribute to tumorigenesis. However, it is unclear how widespread this type of cryptic 3′ss usage is in cancers and what is the full spectrum of genetic mutations that cause such missplicing. To address this issue, we performed an unbiased pan-cancer analysis to identify genetic alterations that lead to the same aberrant splicing as observed with SF3B1 mutations. This analysis identified multiple mutations in another spliceosomal gene, SUGP1, that correlated with significant usage of cryptic 3′ss known to be utilized in mutant SF3B1 expressing cells. Remarkably, this is consistent with recent biochemical studies that identified a defective interaction between mutant SF3B1 and SUGP1 as the molecular defect responsible for cryptic 3′ss usage. Experimental validation revealed that five different SUGP1 mutations completely or partially recapitulated the 3′ss defects. Our analysis suggests that SUGP1 mutations in cancers can induce missplicing identical or similar to that observed in mutant SF3B1 cancers.

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Alsafadi, Samar, Stephane Dayot, Malcy Tarin, Alexandre Houy, Dorine Bellanger, Michele Cornella, Michel Wassef i in. "Genetic alterations of SUGP1 mimic mutant-SF3B1 splice pattern in lung adenocarcinoma and other cancers". Oncogene 40, nr 1 (14.10.2020): 85–96. http://dx.doi.org/10.1038/s41388-020-01507-5.

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AbstractGenes involved in 3′-splice site recognition during mRNA splicing constitute an emerging class of oncogenes. SF3B1 is the most frequently mutated splicing factor in cancer, and SF3B1 mutants corrupt branchpoint recognition leading to usage of cryptic 3′-splice sites and subsequent aberrant junctions. For a comprehensive determination of alterations leading to this splicing pattern, we performed a pan-TCGA screening for SF3B1-specific aberrant acceptor usage. While the most of aberrant 3′-splice patterns were explained by SF3B1 mutations, we also detected nine SF3B1 wild-type tumors (including five lung adenocarcinomas). Genomic profile analysis of these tumors identified somatic mutations combined with loss-of-heterozygosity in the splicing factor SUGP1 in five of these cases. Modeling of SUGP1 loss and mutations in cell lines showed that both alterations induced mutant-SF3B1-like aberrant splicing. Our study provides definitive evidence that genetic alterations of SUGP1 genocopy SF3B1 mutations in lung adenocarcinoma and other cancers.

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Benbarche, Salima, Jose Maria Bello Pineda, Laura Baquero Galvis, Bo Liu, Jeetayu Biswas, Eric Wang, K. Ashley Lyttle i in. "Synthetic Introns Identify the Novel RNA Splicing Factor GPATCH8 As Required for Mis-Splicing Induced By SF3B1 Mutations". Blood 142, Supplement 1 (28.11.2023): 3. http://dx.doi.org/10.1182/blood-2023-179848.

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Disclosures Mutations in the core RNA splicing factor SF3B1 are common across MDS, CLL, and clonal hematopoiesis. Prior studies have elucidated that mutations in SF3B1 result in neomorphic widespread changes in splicing due to usage of aberrant intronic branchpoint nucleotides. However, the molecular basis by which mutant SF3B1 induces mis-splicing is not established and therapeutic means to correct mis-splicing due to mutant SF3B1 do not exist. Recently, the aberrant gain-of-function splicing activity of mutant SF3B1 was harnessed to regulate expression of proteins in a mutant selective manner using synthetic version of endogenous mRNA sequences uniquely recognized by mutant SF3B1. Here, we utilized this technology to engineer a synthetic intron derived from MAP3K7 that interrupts the coding sequence of the fluorescent protein mEmerald such that mutant SF3B1 produces lower mEmerald expression than SF3B1 wild-type (WT) cells (Fig.A). This fluorescent splicing reporter was then used to perform positive enrichment whole genome CRISPR screens to identify genes whose deletion corrects SF3B1 mutant aberrant splicing. GPATCH8 was the single most robust hit. GPATCH8 knockout strongly corrected mis-splicing of both synthetic and endogenous MAP3K7 introns (Fig.A). A previously unexplored protein, GPATCH8 has domains characteristic of RNA splicing factors including a G-patch motif, thought to be important in activating RNA helicases. Interestingly, recent work suggests that mutations in SF3B1 result in mis-splicing by disrupting physical interaction of SF3B1 to the RNA helicase DHX15 via the G-patch domain containing protein SUGP1. We therefore compared SUGP1 to GPATCH8 activity, evaluating first their transcriptome-wide binding sites using TRIBE-seq. We found that both proteins predominantly target intronic sequences over other genomic regions suggesting roles in splicing. RNA-seq of SF3B1 mutant and WT cells with or without GPATCH8/SUGP1 deletion revealed that ~33% of SF3B1 mutant splicing alterations are corrected by GPATCH8 deletion, while ~60% of SF3B1 mutant splicing alterations are recapitulated upon SUGP1 deletion. GPATCH8 regulated splicing events have stronger branchpoints indicating a potential role for GPATCH8 in 3' splice site recognition. To further understand the connection between GPATCH8 and mutant SF3B1, we performed mass spectrometry studies of immunoprecipitated endogenous GPATCH8 in SF3B1 WT and mutant knockin cells. This revealed strong interaction between GPATCH8 and DHX15. GPATCH8 interacts with DHX15 at the same sites previously shown to be occupied by SUGP1 in crystal structures of the SUGP1/DHX15 interaction. These data and further biochemical studies elucidated that GPATCH8 competes with SUGP1 for interaction to DHX15. As such, deletion of GPATCH8 corrects SF3B1 mutant mis-splicing by enhancing the interaction of SUGP1 and DHX15 to the mutant SF3b complex. Given that GPATCH8 is required for a large proportion of the splicing alterations induced by mutant SF3B1, we next evaluated the phenotypic effect of correcting SF3B1 mutant mis-splicing. We first tested the impact of anti-Gpatch8 shRNAs in bone marrow from WT mice as well as animals with conditional knockin of Sf3b1 K700E, K666N, or R625H mutations. While each Sf3b1 mutation results in impaired colony formation of hematopoietic precursors in methylcellulose assays, silencing of Gpatch8 rescued colony formation from hematopoietic precursors of each of the different Sf3b1 mutant mice and was tolerated by normal hematopoietic precursors (Fig.B). Moreover, while CRISPR base-edited knockin of the SF3B1 K700E mutation in adult CD34 + cells impaired erythroid development, this erythroid differentiation defect was rescued by GPATCH8 deletion in the same cells (Fig.B). These data identify GPATCH8 as a novel RNA splicing factor involved in quality control of RNA branchpoint selection whose expression is required for mis-splicing by the different mutant forms of SF3B1. GPATCH8 antagonizes the activity of SUGP1 by competing for interaction with DHX15. These findings suggest that disrupting GPATCH8/DHX15 interaction could have important therapeutic benefit for the multitude of SF3B1 mutant hematopoietic diseases. This study also demonstrates the power of synthetic intronic splicing assays for discovery of trans factors and druggable proteins required by leukemia-associated mutant RNA splicing factors. Abdel-Wahab: AbbVie, Inc.: Consultancy, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Loxo/Lilly: Consultancy; Nurix Therapeutics: Research Funding; Minovia Therapeutics: Research Funding; Amphista Therapeutics: Consultancy; AstraZeneca: Consultancy; Harmonic Discovery: Current holder of stock options in a privately-held company. Figure 1

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Zhang, Jian, Abdullah M. Ali, Yen K. Lieu, Zhaoqi Liu, Jianchao Gao, Raul Rabadan, Azra Raza, Siddhartha Mukherjee i James L. Manley. "Disease-Causing Mutations in SF3B1 Alter Splicing by Disrupting Interaction with SUGP1". Molecular Cell 76, nr 1 (październik 2019): 82–95. http://dx.doi.org/10.1016/j.molcel.2019.07.017.

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Feng, Qing, Keegan Krick, Jennifer Chu i Christopher B. Burge. "Splicing quality control mediated by DHX15 and its G-patch activator SUGP1". Cell Reports 42, nr 10 (październik 2023): 113223. http://dx.doi.org/10.1016/j.celrep.2023.113223.

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Deng, Guo-Xiong, Rui-Xing Yin, Yao-Zong Guan, Chun-Xiao Liu, Peng-Fei Zheng, Bi-Liu Wei, Jin-Zhen Wu i Liu Miao. "Association of the NCAN-TM6SF2-CILP2-PBX4-SUGP1-MAU2 SNPs and gene-gene and gene-environment interactions with serum lipid levels". Aging 12, nr 12 (22.06.2020): 11893–913. http://dx.doi.org/10.18632/aging.103361.

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Liu, Xinglin, Zengchun Wang, Yanping Jiang, Libo Huang, Xuejun Yuan, Yang Li, Ning Jiao, Weiren Yang i Shuzhen Jiang. "Quantitative Proteomic Analysis of Zearalenone Exposure on Uterine Development in Weaned Gilts". Toxins 14, nr 10 (9.10.2022): 692. http://dx.doi.org/10.3390/toxins14100692.

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The aim of this study was to explore the effect of zearalenone (ZEA) exposure on uterine development in weaned gilts by quantitative proteome analysis with tandem mass spectrometry tags (TMT). A total of 16 healthy weaned gilts were randomly divided into control (basal diet) and ZEA3.0 treatments groups (basal diet supplemented with 3.0 mg/kg ZEA). Results showed that vulva size and uterine development index were increased (p < 0.05), whereas serum follicle stimulation hormone, luteinizing hormone and gonadotropin-releasing hormone were decreased in gilts fed the ZEA diet (p < 0.05). ZEA, α-zearalenol (α-ZOL) and β-zearalenol (β-ZOL) were detected in the uteri of gilts fed a 3.0 mg/kg ZEA diet (p < 0.05). The relative protein expression levels of creatine kinase M-type (CKM), atriopeptidase (MME) and myeloperoxidase (MPO) were up-regulated (p < 0.05), whereas aldehyde dehydrogenase 1 family member (ALDH1A2), secretogranin-1 (CHGB) and SURP and G-patch domain containing 1 (SUGP1) were down-regulated (p < 0.05) in the ZEA3.0 group by western blot, which indicated that the proteomics data were dependable. In addition, the functions of differentially expressed proteins (DEPs) mainly involved the cellular process, biological regulation and metabolic process in the biological process category. Some important signaling pathways were changed in the ZEA3.0 group, such as extracellular matrix (ECM)-receptor interaction, focal adhesion and the phosphoinositide 3-kinase–protein kinase B (PI3K-AKT) signaling pathway (p < 0.01). This study sheds new light on the molecular mechanism of ZEA in the uterine development of gilts.

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Arslanow, A., C. S. Stokes, F. Grünhage, F. Lammert i M. Krawczyk. "P1048 : Effects of prosteatogenic TM6SF2 and NCAN/SUGP1 variants on hepatic steatosis and non-invasive markers of liver injury in patients with chronic liver diseases". Journal of Hepatology 62 (kwiecień 2015): S741—S742. http://dx.doi.org/10.1016/s0168-8278(15)31246-0.

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Ghodsian, Nooshin, Erik Abner, Émilie Gobeil, Nele Taba, Alexis St Amand, Nicolas Perrot, Christian Couture i in. "Electronic Health Record-Based Genome-Wide Meta-Analysis Identifies New Susceptibility Loci for Non-Alcoholic Fatty Liver Disease". Journal of the Endocrine Society 5, Supplement_1 (1.05.2021): A501. http://dx.doi.org/10.1210/jendso/bvab048.1024.

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Abstract Background: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease. Observational studies documented associations of NAFLD with several chronic and infectious diseases but whether these associations underlie causal effects is unknown. The molecular mechanisms and genetic architecture of NAFLD are poorly understood. Our objectives were to identify genetic loci associated with NAFLD and determine whether the presence of NAFLD was causally associated with human diseases. Methods: We created a NAFLD genetic instrument through the identification of independent single-nucleotide polymorphisms (SNPs) associated with NAFLD in a meta-analysis of genome-wide association study (GWAS) (6715 cases and 682,748 controls). Using inverse-variance weighted Mendelian Randomization (MR), we investigated the impact of NAFLD on human disease-related phenotypes in the UK Biobank and FinnGen cohorts as well as in the COVID-19 host genetics initiative. Results: We first performed a GWAS meta-analysis of four cohorts and found variants significantly associated with NAFLD (p<5.0E-8) at six genetic loci (MTARC1, GCKR, TRIB1, LMO3, SUGP1 [TM6SF2] and PNPLA3). Using a risk factor informed Bayesian approach (bGWAS), we identify variants at three additional loci (LPL, FTO, and APOE). To determine if the association between NAFLD and human diseases shows evidence of causality, we performed MR across the human disease-related phenome (>800 diseases) using a genetic instrument for NAFLD. Results of these analyses suggest that NAFLD was not causally associated with diseases outside the spectrum of liver diseases. We also found no causal association between genetically predicted NAFLD and COVID-19-related outcomes. Conclusions: This study identified several new genetic loci associated with NAFLD. NAFLD was not causally associated with diseases outside those of the spectrum of liver diseases. This finding suggests that the resolution of NAFLD might not prevent other diseases previously associated with NAFLD.

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Patterton, D., i J. Hapgood. "suGF1 binds in the major groove of its oligo(dG).oligo(dC) recognition sequence and is excluded by a positioned nucleosome core". Molecular and Cellular Biology 14, nr 2 (luty 1994): 1410–18. http://dx.doi.org/10.1128/mcb.14.2.1410-1418.1994.

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We have elsewhere reported the purification of a poly(dG).poly(dC)-binding nuclear protein (suGF1) from sea urchin embryos (J. Hapgood and D. Patterton, Mol. Cell. Biol. 14:this issue, 1994). We proposed that suGF1 may be a member of a family of G-string factors involved in developmental gene regulation, possibly via alterations in chromatin structure. In this article, we characterize the binding of purified suGF1 to 11 contiguous Gs in the H1-H4 intergenic region of a sea urchin early histone gene battery in vitro. It is shown that suGF1-DNA binding is dependent on ionic strength and requires divalent cations. Purified suGF1 forms discrete protein-DNA multimers, consistent with suGF1-suGF1 interactions. In a model for the suGF1-DNA complex derived from our footprinting and methylation interference data, suGF1 contacts the Gs in the major groove as well as one of the bordering phosphate backbones. The data are consistent with the direction of curvature of the DNA in the suGF1-DNA complex being the same as that preferred by the free DNA and exhibited by the DNA when bent around a positioned nucleosome core in vitro. However, on the basis of steric considerations, the binding of suGF1 and that of the histone octamer are predicted to be mutually exclusive. We show that suGF1 is indeed unable to bind to the G string when occupied by a histone octamer located in the major in vitro positioning frame in the H1-H4 intergenic region.

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Rozprawy doktorskie na temat "Sugp1"

Canbezdi, Christine. "Rôle des mutations de SF3B1 et SUGP1 dans l'épissage aberrant des cancers humains". Electronic Thesis or Diss., Université Paris sciences et lettres, 2024. http://www.theses.fr/2024UPSLS049.

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Parmi les gènes d’épissage impliqués dans les cancers, SF3B1 est le plus fréquemment muté dans les hémopathies et certaines tumeurs solides. Les mutations récurrentes de SF3B1 entraînent la reconnaissance d’un site 3’ d’épissage alternatif, aboutissant à des ARNm aberrants avec une rétention partielle d’introns. D’autres mutations de SF3B1 sont retrouvées dans les cancers sans que leurs conséquences soient connues. Par ailleurs, des mutations hypomorphes de SUGP1, retrouvées notamment dans certains adénocarcinomes pulmonaires ont été associées à une signature d’épissage aberrant similaire à celle observée pour les mutants SF3B1. Cependant, le rôle fonctionnel de SUGP1 dans l’épissage aberrant dans les cancers est peu caractérisé.Nous avons utilisé la signature d’épissage aberrant de SF3B1 comme un marqueur de l’impact fonctionnel des mutations de SF3B1. Par modélisation 3D, nous avons ensuite prédit les conséquences de cet impact fonctionnel sur la conformation protéique des mutants SF3B1.Nos résultats suggèrent que les mutations de SF3B1 n’entraînent pas la même pathogénicité dans les cancers selon la position du codon muté et la substitution d’acide aminés. Ceci semble corréler positivement avec le changement de conformation protéique au niveau de la région N-terminale de SF3B1.Pour mieux comprendre la fonction de SUGP1, nous avons généré par CRISPR/Cas9 un modèle isogénique cellulaire présentant une inactivation partielle de SUGP1. Les conséquences fonctionnelles ainsi que la composition du spliceosome en présence du mutant SUGP1 par spectrométrie de masse ont été étudiés.Le modèle CRISPR/Cas9 présentant une inactivation partielle de SUGP1 reproduit les anomalies d’épissage des cancers. Nous avons montré qu’une forte pression de sélection positive existe sur SUGP1, entraînant l’apparition de révertants spontanés. Nos résultats montrent qu’un des révertants sans domaine ULM, mais comportant un domaine G-patch reproduit partiellement ces anomalies d’épissage. Il semble interférer avec la composition du spliceosome, en particulier celle du complexe snRNP U2 et nous permet de comprendre davantage sur la fonction de SUGP1.Dans l’ensemble, ce travail a montré que les conséquences fonctionnelles des mutations de SF3B1 impactent la conformation protéique des mutants SF3B1. Il nous a permis d’affiner le modèle d’action du spliceosome actuel en lien avec SUGP1 et de comprendre sa dynamique en relation avec d’autres partenaires comme SF3B1, de grande importance dans la physiologie et le cancer
Among the splicing genes involved in cancers, SF3B1 is the most frequently mutated in blood diseases and some solid tumors. Recurrent SF3B1 mutations result in recognition of an alternative 3' splice site, resulting in aberrant mRNAs with partial intron retention. Other SF3B1 mutations are found in cancers without their consequences being known. Furthermore, hypomorphic mutations in SUGP1, found especially in some lung adenocarcinomas, have been associated with an aberrant splicing signature similar to that observed for SF3B1 mutants. However, the functional role of SUGP1 in aberrant splicing in cancers is poorly characterized.We used the aberrant splicing signature of SF3B1 as a marker of the functional impact of SF3B1 mutations. Using 3D modeling, we then predicted the consequences of this functional impact on the protein conformation of SF3B1 mutants.Our results reveal that SF3B1 mutations do not cause the same pathogenicity in cancers depending on the position of the mutated codon and the amino acid substitution. This appears to correlate positively with the change in protein conformation at the N-terminal region of SF3B1.To better understand the function of SUGP1, we generated by CRISPR/Cas9 an isogenic cell model exhibiting partial inactivation of SUGP1. The functional consequences as well as the composition of the spliceosome in the presence of the SUGP1 mutant by mass spectrometry were studied.CRISPR/Cas9 model with partial SUGP1 inactivation reproduces splicing abnormalities in cancers. We showed that a strong positive selection pressure exists on SUGP1, leading to the appearance of spontaneous revertants. Our results show that one of the revertants without a ULM domain, but containing a G-patch domain, partially reproduces these splicing abnormalities. It appears to interfere with the composition of the spliceosome, especially U2 snRNP complex, and allows us to understand more about the function of SUGP1.Overall, this work showed that the functional consequences of SF3B1 mutations impact the protein conformation of SF3B1 mutants. It allowed us to refine the current spliceosome action model in relation to SUGP1 and to understand its dynamics in relation to other partners such as SF3B1, of great importance in physiology and cancer

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Scherer, Sonja Daniela. "Protein purification and cDNA cloning of suGF1 : a sea urchin nuclear DNA-binding factor". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/21905.

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The upstream regulatory regions of numerous genes contain contiguous deoxyguanosine residues (G·C-rich sequences) which have been implicated in the regulation of gene expression, since they may involve alterations in their DNA structure, the binding of G-string factors and in some cases even the displacement of a nucleosome positioned over this area. A poly( dG).poly( de)-binding protein (suGF1) has previously been identified and purified on a small scale from embryonic nuclear extracts of the sea urchin Parechinus angulosus (1, 2). suGF1 binds in vitro to the H1-H4 intergenic region of the early histone gene battery, and the recognition site contains 11 contiguous Gs which are incorporated into a positioned nucleosome core in vitro. suGFI may be a member of a family of Gstring factors which could be involved in the developmental regulation of unrelated genes in various organisms. Prior to the commencement of this project no protein or DNA sequence information was available on the protein. The main objective of this thesis was to obtain the eDNA and the primary amino acid sequence for suGFI. Using this information, additional aims were to determine the developmental distribution of the protein and obtain insight into the molecular basis of the regulatory function of suGF 1 by analysis of the primary protein structure and expression of the eDNA.

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Ulker, Fatma Demet. "Active Vibration Control Of Smart Structures". Master's thesis, METU, 2003. http://etd.lib.metu.edu.tr/upload/4/1098409/index.pdf.

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The purpose of this thesis was to design controllers by using H1 and ¹
control strategies in order to suppress the free and forced vibrations of smart structures. The smart structures analyzed in this study were the smart beam and the smart ¯
n. They were aluminum passive structures with surface bonded PZT (Lead-Zirconate-Titanate) patches. The structures were considered in clamped-free con¯
guration. The ¯
rst part of this study focused on the identi¯
cation of nominal system models of the smart structures from the experimental data. For the experimentally identi¯
ed models the robust controllers were designed by using H1 and ¹
-synthesis strategies. In the second part, the controller implementation was carried out for the suppression of free and forced vibrations of the smart structures. Within the framework of this study, a Smart Structures Laboratory was established in the Aerospace Engineering Department of METU. The controller implementations were carried out by considering two di®
erent experimental set-ups. In the ¯
rst set-up the controller designs were based on the strain measurements. In the second approach, the displacement measurements, which were acquired through laser displacement sensor, were considered in the controller design. The ¯
rst two °
exural modes of the smart beam were successfully controlled by using H1 method. The vibrations of the ¯
rst two °
exural and ¯
rst torsional modes of the smart ¯
n were suppressed through the ¹
-synthesis. Satisfactory attenuation levels were achieved for both strain measurement and displacement measurement applications.

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Koues, Olivia I. "The Epigenetic Regulation of Cytokine Inducible Mammalian Transcription by the 26S Proteasome". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/59.

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It is evident that components of the 26S proteasome function beyond protein degradation in the regulation of transcription. Studies in yeast implicate the 26S proteasome, specifically the 19S cap, in the epigenetic regulation of transcription. Saccharomyces cerevisiae 19S ATPases remodel chromatin by facilitating histone acetylation and methylation. However, it is unclear if the 19S ATPases play similar roles in mammalian cells. We previously found that the 19S ATPase Sug1 positively regulates transcription of the critical inflammatory gene MHC-II and that the MHC-II promoter fails to efficiently bind transcription factors upon Sug1 knockdown. MHC-II transcription is regulated by the critical coactivator CIITA. We now find that Sug1 is crucial for regulating histone H3 acetylation at the cytokine inducible MHC-II and CIITA promoters. Histone H3 acetylation is dramatically decreased upon Sug1 knockdown with a preferential loss occurring at lysine 18. Research in yeast indicates that the ortholog of Sug1, Rpt6, acts as a mediator between the activating modifications of histone H2B ubiquitination and H3 methylation. Therefore, we characterized the role the 19S proteasome plays in regulating additional activating modifications. As with acetylation, Sug1 is necessary for proper histone H3K4 and H3R17 methylation at cytokine inducible promoters. In the absence of Sug1, histone H3K4me3 and H3R17me2 are substantially inhibited. Our observation that the loss of Sug1 has no significant effect on H3K36me3 implies that Sug1’s regulation of histone modifications is localized to promoter regions as H3K4me3 but not H3K36me3 is clustered around gene promoters. Here we show that multiple H3K4 histone methyltransferase subunits bind constitutively to the inducible MHC-II and CIITA promoters and that over-expressing one subunit significantly enhances promoter activity. Furthermore, we identified a critical subunit of the H3K4 methyltransferase complex that binds multiple histone modifying enzymes, but fails to bind the CIITA promoter in the absence of Sug1, implicating Sug1 in recruiting multi-enzyme complexes responsible for initiating transcription. Finally, Sug1 knockdown maintains gene silencing as elevated levels of H3K27 trimethylation are observed upon Sug1 knockdown. Together these studies strongly implicate the 19S proteasome in mediating the initial reorganization events to relax the repressive chromatin structure surrounding inducible genes.

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Bhat, Kavita Purnanda. "Roles of the Ubiquitin-Proteasome System and Mono-ubiquitination in Regulating MHC class II Transcription". Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/biology_diss/82.

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Major Histocompatibility Complex (MHC) class II molecules are indispensable arms of the im-mune system that present extracellular antigens to CD4+T cells and initiate the adaptive immune response. MHC class II expression requires recruitment of a master regulator, the class II trans-activator (CIITA). How this master transcriptional regulator is recruited, stabilized and degraded is unknown. The 26S proteasome, a master regulator of protein degradation, is a multi-subunit complex composed of a 20S core particle capped on one or both ends by 19S regulatory particles. Previous findings have linked CIITA and MHC class II transcription to the ubiquitin proteasome system (UPS) as mono-ubiquitination of CIITA increases its transactivity whereas poly-ubiquitination targets CIITA for degradation. Increasing evidence indicates individual ATPase subunits of the 19S regulator play non-proteolytic roles in transcriptional regulation and histone modification. Our initial observations indicate proteasome inhibition decreases CIITA transac-tivity and MHC class II expression without affecting CIITA expression levels. Following cyto-kine stimulation, the 19S ATPase Sug1 associates with CIITA and with the MHC class II enhan-ceosome complex. Absence of Sug1 reduces promoter recruitment of CIITA and proteasome inhibition fails to restore CIITA binding, indicating Sug1 is required for CIITA mediated MHC class II expression. Furthermore, we identify a novel N-terminal 19S ATPase binding domain (ABD) within CIITA. The ABD of CIITA lies within the Proline/Serine/Threonine (P/S/T) re-gion of CIITA and encompasses a majority of the CIITA degron sequence. Absence of the ABD increases CIITA half-life, but blocks MHC class II surface expression, indicating that CIITA requires interaction with the 19S ATPases for both its deployment and destruction. Finally, we identify three degron proximal lysine residues, lysines (K): K315, K330 and K333, and a phosphorylation site, serine (S), S280, located within the CIITA degron, that regulate CIITA ubiquitination, stability and MHC class II expression. These are the first lysine residues identified as sites of CIITA ubiquitination that are essential for MHC class II expression. These observations increase our understanding of the role of the UPS in modulating CIITA mediated MHC class II transcription and will facilitate the development of novel therapies involving manipulation of MHC class II gene expression.

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Kylarová, Salome. "Příprava a charakterizace vazebných partnerů fosducinu". Master's thesis, 2013. http://www.nusl.cz/ntk/nusl-324646.

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AABBSSTTRRAACCTT Phosducin (Pdc) is a highly conserved acidic phosphoprotein, which plays an important role in the regulation of G-protein signalization in intact retina. It binds to Gβγ dimer of heterotrimeric G-protein transducin thereby decreases the pool of available transducin resulting in modulation of signal. Function of phosducin is negatively regulated by its phosphorylation followed by interaction with the 14-3-3 protein. Besides this established way of regulation, we were interested in other putative interaction partners of phosducin, like SUG1 and CRX. SUG1 is a subunit of 26S proteasome with a large scale of biological functions, especially a degradation of many transription factors. Its role in regulation of phosducin is still unclear, but is probably involved in targeting of phosducin to 26S proteasome for its degradation. Subsequently, we prepared four different expression constructs of full-length protein in order to find the best expression and purification strategy. These results suggest that all purified fusion proteins of SUG1 form stable and soluble high molecular weight oligomers. This behaviour was confirmed by dynamic light scattering and analytical ultracentrifugation measurements. In addition, this observation is consistent with previous studies of its bacterial counterpart, PAN...

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Maganti, Nagini. "Role of 26S Proteasome and Regulator of G-Protein Signaling 10 in Regulating Neuroinflammation in the Central Nervous System". 2015. http://scholarworks.gsu.edu/biology_diss/162.

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Major histocompatibility complex molecules (MHCII) are cell surface glycoproteins that present extracellular antigens to CD4+ T lymphocytes and initiate adaptive immune responses. Apart from their protective role, overexpression of MHCII contributes to autoimmune disorders where the immune system attacks our own tissues. Autoimmune diseases are characterized by self-reactive responses to autoantigens, promoting tissue damage, inflammation mediated by proinflammatory cytokines, autoreactive lymphocytes, and autoantibodies. MHCII molecules are tightly regulated at the level of transcription by Class II transactivator (CIITA). CIITA associates with an enhanceosome complex at MHCII promoters and regulates the expression of MHCII. It is thus crucial to understand the regulation of CIITA expression in order to regulate MHCII in autoimmune diseases. Our lab has shown that the 19S ATPases of the 26S proteasome associate with MHCII and CIITA promoters and play important roles in gene transcription, regulate covalent modifications to histones, and are involved in the assembly of activator complexes in mammalian cells. The mechanisms by which the proteasome influences transcription remain unclear. Here, we define novel roles of the 19S ATPases Sug1, S7, and S6a in expression of CIITApIV genes. These ATPases are recruited to CIITApIV promoters and coding regions, interact with the elongation factor PTEFb, and with Ser5 phosphorylated RNA Pol II. Both the generation of CIITApIV transcripts and efficient recruitment of RNA Pol II to CIITApIV are negatively impacted by knockdown of 19S ATPases. Alternatively, inflammation is also suppressed via the Regulator of G-protein signaling 10 (RGS10) in microglial cells which express high levels of RGS10 and promote homeostasis in the central nervous system. However, chronic activation of microglial cells leads to release of cytokines which cause neuroinflammation. Our investigation of roles played by RGS10 in chronically activated microglial cells indicates that RGS10 binds to promoters of IL-1β, and TNF-α and regulates these genes, while the molecular mechanism remains to be investigated. Together, our observations indicate roles for the UPS in modulating gene expression and for RGS10 in regulating proinflammatory cytokines in microglial cells, each of which provides novel therapeutic targets to combat inflammation in autoimmune and neurodegenerative diseases.

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Książki na temat "Sugp1"

Southeast Asian Fisheries Development Center. Aquaculture Dept. Library & Documentation Services. i Brackishwater Aquaculture Information System, red. Sugpo and other Philippine penaeids: A classified list of materials available at the SEAFDEC Aquaculture Department Library. Tigbauan, Iloilo, Philippines: Brackishwater Aquaculture Information System, SEAFDEC Aquaculture Dept., 1985.

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Southeast Asian Fisheries Development Center. Aquaculture Dept. Library. Sugpo and other Philippine penaeids: A classified list of materials available at the SEAFDEC Aquaculture Department Library. Tigbauan, Iloilo, Philippines: Brackishwater Aquaculture Information System, SEAFDEC Aquaculture Dept., 1987.

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Weisweiller. The Foreign Exchange Man Supp1. Prentice Hall Europe (a Pearson Education company), 1991.

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Staff, Houghton Mifflin Company. Houghton Mifflin Reading Leveled Readers: Tres Kit Lang Supp1. 1-1. 2. Houghton Mifflin Harcourt Publishing Company, 2003.

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Houghton Mifflin Company. Houghton Mifflin Reading Leveled Readers: Tres Kit Lang Supp1. 1-1. 5. Houghton Mifflin Harcourt Publishing Company, 2003.

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Financial Market Trends. OECD, 2005. http://dx.doi.org/10.1787/fmt-v2005-sup1-en.

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OECD Economic Outlook, Interim Report September 2011. OECD, 2011. http://dx.doi.org/10.1787/eco_outlook-v2011-sup1-en.

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Perspectives économiques de l'OCDE, Rapport intermédiaire septembre 2011. OECD, 2011. http://dx.doi.org/10.1787/eco_outlook-v2011-sup1-fr.

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OECD Economic Outlook, Interim Report September 2012. OECD, 2012. http://dx.doi.org/10.1787/eco_outlook-v2012-sup1-en.

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Perspectives économiques de l'OCDE, Rapport intermédiaire septembre 2012. OECD, 2012. http://dx.doi.org/10.1787/eco_outlook-v2012-sup1-fr.

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Części książek na temat "Sugp1"

Goebel, Zane. "Superdiversity". W Handbook of Pragmatics, 221–38. Amsterdam: John Benjamins Publishing Company, 2018. http://dx.doi.org/10.1075/hop.21.sup1.

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"SUG1". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1896. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_16334.

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Streszczenia konferencji na temat "Sugp1"

Fabregas, Aleta C., Debrelie Cruz i Mark Daniel Marmeto. "SUGPO". W the 6th International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3301551.3301574.

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Marquez, Guillermo, Lihong V. Wang, Mehrube Mehrubeoglu i Nasser Kehtarnavaz. "Imaging obliquely illuminated skin lesions for skin cancer detection". W Biomedical Optical Spectroscopy and Diagnostics. Washington, D.C.: OSA, 2000. http://dx.doi.org/10.1364/bosd.2000.sug1.

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Yang, Shao, Darryl Keenan i Marla Dowell. "UV Pulse Response Nonlinearity of Two Si Photodiodes". W Asia Optical Fiber Communication and Optoelectronic Exposition and Conference. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/aoe.2008.sug1.

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Mazzali, Claudio, i Ming-Jun Li. "Recent Developments in Optical Fiber Technology and Their Impact Opening New Application Spaces". W Asia Optical Fiber Communication and Optoelectronic Exposition and Conference. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/aoe.2008.sup1.

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Mizuno, Hitoshi, Akihiro Horii, Hiroki Hibino, Mamoru Kaneko, Kazuhiro Gono, Hirokazu Nishimura i Tetsuo Nonami. "New imaging technologies for endoscopic applications". W Biomedical Topical Meeting. Washington, D.C.: OSA, 2002. http://dx.doi.org/10.1364/bio.2002.sug1.

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Page, Álvaro, Nicolás Jara, José Luis Abad i José Navarro. "Validación de los marcadores ArUco para el análisis de movimientos humanos". W 11 Simposio CEA de Bioingeniería. València: Editorial Universitat Politècnica de València, 2019. http://dx.doi.org/10.4995/ceabioing.2019.10029.

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En los últimos años se han publicado numerosos trabajos sobre el empleo de técnicas de bajo coste para el análisis de movimientos humanos, especialmente mediante sensores inerciales [1]. Menos esfuerzos se han realizado en la línea de otras técnicas basadas en video-análisis, donde la mayoría de trabajos se refieren al análisis de movimientos planos con una cámara [2]. Sin embargo, en el campo de la robótica se vienen usando desde hace tiempo sistemas de posicionado mediante marcadores de realidad aumentada (AR). Estos sistemas permiten analizar, en tiempo real y con una única cámara de video, la posición y orientación de objetos con precisión suficiente para su uso en muchas aplicaciones biomecánicas [3]. En particular, la librería ARUCO [4] permite analizar movimientos de varios marcadores de manera rápida y eficiente, lo que permite aplicarlos al análisis de varios segmentos corporales en tiempo real. En este trabajo se analiza la precisión de los marcadores ARUCO en la medida de ángulos y desplazamientos, comparando los movimientos medidos con el sistema con dos técnicas de precisión: encoders de desplazamientos lineales y giros, para las medidas estáticas, y un sistema de videofotogrametría de precisión, para las medidas en movimiento. Los resultados muestran que los marcadores pueden medir desplazamientos con errores estándar del orden de 1 mm en los desplazamientos paralelos al plano de la cámara y del orden de 3 mm en profundidad. Los errores angulares son inferiores a 0.5º en los giros en el plano de la cámara y del orden de 1º en los giros alrededor de ejes paralelos a dicho plano. Estos errores son mucho menores que los asociados a la variabilidad humana, por lo que sería posible utilizar este tipo de marcadores para numerosas aplicaciones biomecánicas. REFERENCIAS [1] Picerno, P. (2017). 25 years of lower limb joint kinematics by using inertial and magnetic sensors: a review of methodological approaches. Gait & Posture, 51, 239-246. [2] Otín, C. et al.(2016). Análisis de habilidades deportivas mediante el uso del software Kinovea. In Simbiosis del aprendizaje con las tecnologías: experiencias innovadoras en el ámbito hispano (pp. 125-134). Prensas Universitarias de Zaragoza. [3] Parrilla, E. et al. (2013). Ankle 3D-kinematics measurement by using a single camera and AR-markers. Footwear Science, 5(sup1), S73-S74. [4] Munoz-Salinas, R. (2012). ArUco: a minimal library for augmented reality applications based on opencv. Universidad de Córdoba.

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