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Artykuły w czasopismach na temat "Hsp31"

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Rasouly, Aviram, Yotam Shenhar i Eliora Z. Ron. "Thermoregulation of Escherichia coli hchA Transcript Stability". Journal of Bacteriology 189, nr 15 (25.05.2007): 5779–81. http://dx.doi.org/10.1128/jb.00453-07.

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ABSTRACT The conserved chaperone Hsp31 of Escherichia coli is transcribed at low temperatures by σS and repressed by H-NS, whereas at high temperature, transcription is by σ70 independently of both σS and H-NS. Here we present evidence for an additional, novel, temperature-dependent control of Hsp31 expression by increased transcript stability.
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Mujacic, Mirna, i Fran�ois Baneyx. "Chaperone Hsp31 Contributes to Acid Resistance in Stationary-Phase Escherichia coli". Applied and Environmental Microbiology 73, nr 3 (8.12.2006): 1014–18. http://dx.doi.org/10.1128/aem.02429-06.

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ABSTRACT Hsp31, the product of the σS- and σD-dependent hchA gene, is a heat-inducible chaperone implicated in the management of protein misfolding at high temperatures. We show here that Hsp31 plays an important role in the acid resistance of starved Escherichia coli but that it has little influence on oxidative-stress survival.
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Subedi, Krishna P., Dongwook Choi, Insook Kim, Bumchan Min i Chankyu Park. "Hsp31 of Escherichia coli K-12 is glyoxalase III". Molecular Microbiology 81, nr 4 (6.07.2011): 926–36. http://dx.doi.org/10.1111/j.1365-2958.2011.07736.x.

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Hansberg, Wilhelm, Teresa Nava-Ramírez, Pablo Rangel-Silva, Adelaida Díaz-Vilchis i Aydé Mendoza-Oliva. "Large-Size Subunit Catalases Are Chimeric Proteins: A H2O2 Selecting Domain with Catalase Activity Fused to a Hsp31-Derived Domain Conferring Protein Stability and Chaperone Activity". Antioxidants 11, nr 5 (17.05.2022): 979. http://dx.doi.org/10.3390/antiox11050979.

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Bacterial and fungal large-size subunit catalases (LSCs) are like small-size subunit catalases (SSCs) but have an additional C-terminal domain (CT). The catalytic domain is conserved at both primary sequence and structural levels and its amino acid composition is optimized to select H2O2 over water. The CT is structurally conserved, has an amino acid composition similar to very stable proteins, confers high stability to LSCs, and has independent molecular chaperone activity. While heat and denaturing agents increased Neurospora crassa catalase-1 (CAT-1) activity, a CAT-1 version lacking the CT (C63) was no longer activated by these agents. The addition of catalase-3 (CAT-3) CT to the CAT-1 or CAT-3 catalase domains prevented their heat denaturation in vitro. Protein structural alignments indicated CT similarity with members of the DJ-1/PfpI superfamily and the CT dimers present in LSCs constitute a new type of symmetric dimer within this superfamily. However, only the bacterial Hsp31 proteins show sequence similarity to the bacterial and fungal catalase mobile coil (MC) and are phylogenetically related to MC_CT sequences. LSCs might have originated by fusion of SSC and Hsp31 encoding genes during early bacterial diversification, conferring at the same time great stability and molecular chaperone activity to the novel catalases.
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Zhang, Kai, Kuikui Jiang, Ruoxi Hong, Fei Xu, Wen Xia, Ge Qin, Kaping Lee i in. "Identification and characterization of critical genes associated with tamoxifen resistance in breast cancer". PeerJ 8 (4.12.2020): e10468. http://dx.doi.org/10.7717/peerj.10468.

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Background Tamoxifen resistance in breast cancer is an unsolved problem in clinical practice. The aim of this study was to determine the potential mechanisms of tamoxifen resistance through bioinformatics analysis. Methods Gene expression profiles of tamoxifen-resistant MCF-7/TR and MCF-7 cells were acquired from the Gene Expression Omnibus dataset GSE26459, and differentially expressed genes (DEGs) were detected with R software. We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses using Database for Annotation, Visualization and Integrated Discovery. A protein–protein interaction (PPI) network was generated, and we analyzed hub genes in the network with the Search Tool for the Retrieval of Interacting Genes database. Finally, we used siRNAs to silence the target genes and conducted the MTS assay. Results We identified 865 DEGs, 399 of which were upregulated. GO analysis indicated that most genes are related to telomere organization, extracellular exosomes, and binding-related items for protein heterodimerization. PPI network construction revealed that the top 10 hub genes—ACLY, HSPD1, PFAS, GART, TXN, HSPH1, HSPE1, IRAS, TRAP1, and ATIC—might be associated with tamoxifen resistance. Consistently, RT-qPCR analysis indicated that the expression of these 10 genes was increased in MCF-7/TR cells comparing with MCF-7 cells. Four hub genes (TXN, HSPD1, HSPH1 and ATIC) were related to overall survival in patients who accepted tamoxifen. In addition, knockdown of HSPH1 by siRNA may lead to reduced growth of MCF-7/TR cell with a trend close to significance (P = 0.07), indicating that upregulation of HSPH1 may play a role in tamoxifen resistance. Conclusion This study revealed a number of critical hub genes that might serve as therapeutic targets in breast cancer resistant to tamoxifen and provided potential directions for uncovering the mechanisms of tamoxifen resistance.
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Kim, Jihong, Dongwook Choi, Chankyu Park i Kyoung-Seok Ryu. "Backbone resonance assignments of the Escherichia coli 62 kDa protein, Hsp31". Biomolecular NMR Assignments 11, nr 2 (3.03.2017): 159–63. http://dx.doi.org/10.1007/s12104-017-9739-6.

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Kim, Jihong, Dongwook Choi, So-Young Cha, Young-Mee Oh, Eunha Hwang, Chankyu Park i Kyoung-Seok Ryu. "Zinc-mediated Reversible Multimerization of Hsp31 Enhances the Activity of Holding Chaperone". Journal of Molecular Biology 430, nr 12 (czerwiec 2018): 1760–72. http://dx.doi.org/10.1016/j.jmb.2018.04.029.

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Choi, Dongwook, Kyoung-Seok Ryu i Chankyu Park. "Structural alteration of Escherichia coli Hsp31 by thermal unfolding increases chaperone activity". Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1834, nr 2 (luty 2013): 621–28. http://dx.doi.org/10.1016/j.bbapap.2012.11.006.

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Hasim, Sahar, Nur Ahmad Hussin, Fadhel Alomar, Keshore R. Bidasee, Kenneth W. Nickerson i Mark A. Wilson. "A Glutathione-independent Glyoxalase of the DJ-1 Superfamily Plays an Important Role in Managing Metabolically Generated Methylglyoxal in Candida albicans". Journal of Biological Chemistry 289, nr 3 (3.12.2013): 1662–74. http://dx.doi.org/10.1074/jbc.m113.505784.

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Methylglyoxal is a cytotoxic reactive carbonyl compound produced by central metabolism. Dedicated glyoxalases convert methylglyoxal to d-lactate using multiple catalytic strategies. In this study, the DJ-1 superfamily member ORF 19.251/GLX3 from Candida albicans is shown to possess glyoxalase activity, making this the first demonstrated glutathione-independent glyoxalase in fungi. The crystal structure of Glx3p indicates that the protein is a monomer containing the catalytic triad Cys136-His137-Glu168. Purified Glx3p has an in vitro methylglyoxalase activity (Km = 5.5 mm and kcat = 7.8 s−1) that is significantly greater than that of more distantly related members of the DJ-1 superfamily. A close Glx3p homolog from Saccharomyces cerevisiae (YDR533C/Hsp31) also has glyoxalase activity, suggesting that fungal members of the Hsp31 clade of the DJ-1 superfamily are all probable glutathione-independent glyoxalases. A homozygous glx3 null mutant in C. albicans strain SC5314 displays greater sensitivity to millimolar levels of exogenous methylglyoxal, elevated levels of intracellular methylglyoxal, and carbon source-dependent growth defects, especially when grown on glycerol. These phenotypic defects are complemented by restoration of the wild-type GLX3 locus. The growth defect of Glx3-deficient cells in glycerol is also partially complemented by added inorganic phosphate, which is not observed for wild-type or glucose-grown cells. Therefore, C. albicans Glx3 and its fungal homologs are physiologically relevant glutathione-independent glyoxalases that are not redundant with the previously characterized glutathione-dependent GLO1/GLO2 system. In addition to its role in detoxifying glyoxals, Glx3 and its close homologs may have other important roles in stress response.
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Nava-Ramírez, Teresa, Sammy Gutiérrez-Terrazas i Wilhelm Hansberg. "The Molecular Chaperone Mechanism of the C-Terminal Domain of Large-Size Subunit Catalases". Antioxidants 12, nr 4 (30.03.2023): 839. http://dx.doi.org/10.3390/antiox12040839.

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Large-size subunit catalases (LSCs) have an additional C-terminal domain (CT) that is structurally similar to Hsp31 and DJ-1 proteins, which have molecular chaperone activity. The CT of LSCs derives from a bacterial Hsp31 protein. There are two CT dimers with inverted symmetry in LSCs, one dimer in each pole of the homotetrameric structure. We previously demonstrated the molecular chaperone activity of the CT of LSCs. Like other chaperones, LSCs are abundant proteins that are induced under stress conditions and during cell differentiation in bacteria and fungi. Here, we analyze the mechanism of the CT of LSCs as an unfolding enzyme. The dimeric form of catalase-3 (CAT-3) CT (TDC3) of Neurospora crassa presented the highest activity as compared to its monomeric form. A variant of the CAT-3 CT lacking the last 17 amino acid residues (TDC3Δ17aa), a loop containing hydrophobic and charged amino acid residues only, lost most of its unfolding activity. Substituting charged for hydrophobic residues or vice versa in this C-terminal loop diminished the molecular chaperone activity in all the mutant variants analyzed, indicating that these amino acid residues play a relevant role in its unfolding activity. These data suggest that the general unfolding mechanism of CAT-3 CT involves a dimer with an inverted symmetry, and hydrophobic and charged amino acid residues. Each tetramer has four sites of interaction with partially unfolded or misfolded proteins. LSCs preserve their catalase activity under different stress conditions and, at the same time, function as unfolding enzymes.
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Rozprawy doktorskie na temat "Hsp31"

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Quigley, Paulene. "Structural studies of the chaperone Hsp31 from Escherichia coli /". Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/8696.

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Mujacic, Mirna. "Characterization of regulation and expression patterns of Escherichia coli Hsp31 protein /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8119.

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Andrade, Warne Pedro de. "Análise da expressão dos genes TRAP1, HSPB1, HSPD1, HSPA1L e HSPA1A em amostras de câncer epitelial de ovário implicações no prognóstico e na resistência a quimioterapia baseada em platina /". Botucatu, 2018. http://hdl.handle.net/11449/154391.

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Orientador: Agnaldo Lopes da Silva Filho
Resumo: Introdução: As proteínas de choque térmico (“Heat Shock Proteins”) são produzidas em resposta ao estresse patofisiológico nas células animais e não só fazem parte de várias etapas da carcinogênese, atuando principalmente como agentes antiapoptóticos, como também estão implicadas em mecanismos de resistência à quimioterapia em vários tipos de tumores. Objetivo: O presente estudo visa comparar a expressão dos genes TRAP1, HSPB1, HSPD1, HSPA1L e HSPA1A nas amostras de CEO (no tumor primário ou na metástase) com a expressão dos mesmos em amostras de tumores ovarianos benignos e tecido ovariano normal e correlacionar a expressão gênica com o prognóstico das pacientes e com a resistência ao tratamento com platina. Métodos: Foram avaliadas amostras de 51 pacientes operadas no Hospital Vera Cruz, entre os anos de 2008 a 2011, divididas em quatro grupos: CEO primário (n = 14), CEO metastático (n = 11), cistoadenoma seroso ovariano (n = 07) e ovário normal (n = 19). Utilizou-se a técnica de qRT-PCR para determinar o perfil de expressão dos genes. Resultados: As pacientes incluídas neste estudo apresentavam idade média de 56,75 anos. Não houve diferença significativa (valor-P> 0,050) na comparação entre a expressão dos genes e os grupos estudados. Os genes HSPA1A, HSPA1L e TRAP1 foram subexpressos e se diferiram significativamente dos genes em indivíduos com ovário normal. A expressão dos genes analisados não correlacionou se com as variáveis quantitativas, como idade, menarca, e tempo ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Heat Shock Proteins are produced in response to pathophysiological stress and take part in several stages of carcinogenesis, acting primarily as anti-apoptotic agents. They are also implicated in resistance to chemotherapy in several types of tumors. Herein we correlated the expression of genes encoding these proteins and the clinical and pathological aspects of patients with ovarian cancer (OC). METHODS: 51 patients included in the study were divided into four groups: those with primary EOC (n = 14), metastatic EOC (n = 11), ovarian serous cystadenoma (n = 7), with no evidence of ovarian malignancy or control (n = 11). The 57 tumor samples obtained were submitted to RNA extraction and reverse transcription. qRT-PCR was performed to compare the expression of TRAP1, HSPB1, HSPD1, HSPA1A and HSPA1L in primary and HSP60, HSP70, HSPA1L genes did not differ among the groups (p-value> 0.050) .HSPA1A, HSPA1L and TRAP1 we underexpressed in the primary and metastatic EOC groups with HSPA1L showing the lowest expression with compare with normal ovary tissue. TRAP1 expression was higher in tumors at stage I/II than at stages III/IV. Grade II subjects showed higher HSPB1 expression. There was no correlation between HSPs expression and age, menarche, parity, period after menopause initiation and CA-125. HSPA1A gene was negatively correlated with the risk of dying of OC. There was no differences between HSP expression gene evaluated and overall and disease-free survival. In conclusion, we ... (Complete abstract click electronic access below)
Mestre
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Smith, Carly M. "HSPC1 inhibitors and their use in Chronic Lymphocytic Leukaemia". Thesis, University of Chester, 2015. http://hdl.handle.net/10034/617678.

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HSPC1 (Hsp90), a member of the anti-apoptotic Heat Shock Protein (HSP) family appears to play a pivotal role in the development and maintenance of several tumour cell characteristics and as a result has become a target for novel anti-cancer therapies. HSPC1 inhibitors have been tested in clinical trials on a wide variety of cancer types with moderate success. However, despite recent advantages in HSPC1 inhibitor development, the effects of these drugs are not consistent. A number of factors may play a role in determining cell sensitivity to these inhibitors. As Chronic Lymphocytic Leukaemia (CLL) is such a heterogeneous disease with great variation in baseline HSP levels and other proteins amongst the patient cohort, it would not be unreasonable to assume that HSPC1 inhibitors may have varying success as a treatment strategy for this disease. The present study examined the effects of four HSPC1 inhibitors on primary CLL cells, as well as cells from healthy control subjects, and analysed a number of HSPC1 client proteins to assess the efficacy of these inhibitors. Great variation in cellular response to these drugs was observed in both CLL and healthy control subjects. Analysis of HSPC1 client proteins in these cells including ZAP-70, Akt, NF-kB and HSPA1A, revealed that HSPC1 inhibitors do not effect client protein levels in all samples. The results suggest that these inhibitors should not be considered as a universal treatment strategy for CLL and provide a basis for further study into elucidating the mechanisms behind HSPC1 inhibitor resistance. The final aim of this work was to investigate the role of the microenvironment in CLL progression, where a co-culture system was used as an in-vitro tool. Whilst consistent data was obtained using cell lines, and showed that microenvironmental factors promoted resistance to HSPC1 inhibitors, use of primary CLL cells in this model produced inconsistent data, again highlighting the heterogeneity of the disease.
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PATEL, VIJAY LAXMAN. "ARABIDOPSIS HSP21 AND MSRB1/MSRB2 IN PLANT STRESS TOLERANCE". Thesis, The University of Arizona, 2008. http://hdl.handle.net/10150/192201.

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Silva, Fábio Fernando Alves da. "Avaliação do papel de HSPB1 na modulação da autofagia induzida por PRL em células-beta". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24082018-092045/.

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O diabetes mellitus tipo 1 é uma doença metabólica, caracterizada pela desregulação glicêmica, que ocorre devido a um ataque autoimune. A insulinoterapia é o tratamento clássico para o DM1. Contudo, alguns pacientes que apresentam essa doença não respondem de forma eficiente a este tratamento e apresentam episódios frequentes de hipoglicemia severa e despercebida (pacientes hiperlábeis). Essas complicações comprometem de forma significativa a qualidade de vida dessas pessoas. O transplante de ilhotas é uma importante alternativa para o tratamento de pacientes hiperlábeis com DM1. No entanto, essa terapia apresenta restrições como a necessidade de mais de um doador por transplante e significativa morte das ilhotas devido ao estresse provocado pelo procedimento de isolamento, além da morte promovida pelo sistema imune do paciente nos primeiros momentos pós-transplante. A autofagia é um mecanismo de reciclagem de componentes citoplasmáticos que é fundamental para a homeostase celular. Em condições de estresse, este mecanismo é ativado acima do seu nível basal, promovendo a degradação de agregados proteicos e organelas defeituosas, evitando assim, danos celulares que comprometam a viabilidade da célula. Trabalhos realizados por nosso grupo têm mostrado a citoproteção que PRL promove em células-beta, reduzindo a apoptose induzida por citocinas pró-inflamatórias. Também demonstramos o papel essencial de HSPB1 na inibição de apoptose induzida por PRL após o tratamento com citocinas. Além disso, resultados recentes de nosso laboratório mostraram um aumento nos níveis de autofagia em células-beta após sua exposição a citocinas, bem como uma restauração a níveis normais na presença de PRL. Visando um melhor entendimento do papel da PRL na modulação da autofagia em células-beta, o objetivo desse projeto foi estudar se HSPB1 também é essencial no mecanismo de regulação da autofagia induzido por PRL.Para tal, fizemos experimentos em modelos de células-beta MIN6, MIN6 silenciadas para HSPB1 (MIN6-shHSPB1) e MIN6 com sequencia short hairpin aleatória (MIN6- SsC), medindo a morte celular através de ensaios de viabilidade, e ensaios de western blot para avaliar os níveis de marcadores de autofagia e fluxo autofágico (degradação de autofagossomos), tratando as células com citocinas, prolactina e indutores ou inibidores de autofagia. Os resultados mostraram que a modulação da autofagia ocasionada pela prolactina em células-beta se dá, em parte, através de HSPB1. O tratamento com prolactina foi capaz de inibir a morte celular induzida por citocinas, mesmo na presença de cloroquina, um bloqueador de autofagia, o que nos levou a concluir que a autofagia não é uma via envolvida na citoproteção de células beta induzida por PRL. Os resultados gerados nesse estudo contribuíram para uma melhor compreensão dos eventos moleculares induzidos por PRL em células-beta, e poderão permitir a inferência de novas abordagens que melhorem a citoproteção, cultura e transplante dessas células em pacientes com diabetes tipo 1.
Type 1 diabetes mellitus is a metabolic disease characterized by glycemic dysregulation, which occurs due to an autoimmune destruction of beta-cells. Insulin therapy is the gold standard treatment for DM1. However, some DM1 patients do not respond efficiently to this treatment and suffer frequent episodes of severe hypoglycemia unawareness. Since this complication jeopardizes the quality of life of these people, Islet transplantation is a therapeutic alternative indicated to treat these patients. However, besides the lack of enough organ donors, the loss of beta cells during both the isolation as well as the infusion of islets into the recipient induce a great estresse and thus a significant cell death is one of the drawbacks of this procedure. Autophagy is a mechanism of recycling cytoplasmic components and is essential for cellular homeostasis. Under estresse conditions, this mechanism is activated above basal levels, promoting the degradation of protein aggregates and defective organelles, thus avoiding cell damage that could compromise cell viability. Studies carried out by our group have shown not only that PRL promotes cytoprotection in beta-cells, reducing pro-inflammatory cytokines-induced apoptosis, but also that HSPB1 plays an essential role in this inhibition of apoptosis mediated by PRL after treatment with cytokines. Moreover, recent results from our laboratory showed an increase in autophagy levels in beta-cells after exposure to cytokines, as well as a restauration to normal levels in the presence of PRL. In order to better understand the role of PRL in the modulation of autophagy in these cells, the aim of this project is to study whether HSPB1 is also essential in the mechanism of autophagy regulation induced by PRL. Using MIN6 beta cell models where HSPB1 was silenced (MIN6-shHSPB1) or not (MIN6-SsC), we studied cell death by viability assays. Moreover, western blot assays were performed in order to assess levels of autophagy and autophagic flux markers in the cells.Our results showed that HSPB1 in one of the mediators of PRL-induced modulation of autophagy. Nevertheless, since hormonal treatment was still able to inhibit cytokinesinduced cell death even in the presence of chloroquin, an autophagy blocker, we conclude that autophagy is not a signaling pathway involved in PRl-induced beta-cell cytoprotection. Altogether, the results shown in this study may help to increase the knowledge of the molecular events induced by PRL in beta-cells, and may allow to infer new approaches to improve cytoprotection, culture and transplantation of these cells into type 1 diabetic patients.
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Bissonnette, Lyne. "Identification de déterminants moléculaires impliqués dans l'activation et le largage de hSPC1/furine". Mémoire, Université de Sherbrooke, 2003. http://savoirs.usherbrooke.ca/handle/11143/3327.

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SPC1/furine est une protéase à sérine active dépendante du Ca[indice supérieur ++] qui est membre de la famille des convertases de mammifères et dont l'homologue bactérien est la subtilisine. Elle est impliquée dans la maturation de plusieurs précurseurs protéiques tels que le prorécepteur à l'insuline, le pro-[bêta]-NGF, le pro-BMP-1 et la pro-fibrilline, les deux derniers étant des substrats de la matrice extracellulaire. Nous avons voulu identifier de nouveaux déterminants du pro-domaine de hSPC1 impliqués dans son auto-activation ainsi que d'autres déterminants moléculaires responsables et nécessaires au largage de l'enzyme dont la forme soluble pourrait cliver des substrats matriciels. Les études ont donc été divisées en deux parties. (1) Une étude d'homologie de séquence entre les pro-domaines des convertases a permis d'identifier des résidus conservés. (2) SPC1 est une protéine transmembranaire de type I dont une forme soluble est générée suite à son largage."--Résumé abrégé par UMI.
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Samsel, Kara Ann. "The Role of Chloroplast-localized HSP21 in the Stress Responses of Arabidopsis Thaliana". Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146645.

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Heat shock proteins (HSPs) are a ubiquitous family of protein chaperones, which prevent irreversible protein aggregation. HSPs help confer thermotolerance to organisms and can protect against other environmental stresses, such as oxidative stress. Expression levels of HSPs increase during exposure to these stresses. Small heat shock proteins (sHSPs) bind to denaturing protein to prevent aggregation. Since sHSPs are ATP-independent, ATP-dependent chaperones are involved in actively refolding proteins after release from sHSPs. Plants, including the model organism Arabidopsis thaliana, contain multiple HSPs, which are localized to the cytosol, chloroplasts, mitochondria, the nucleus, peroxisomes, and ER. This project focuses on the function of chloroplast-localized Hsp21, which is encoded by a single nuclear gene, making it amenable to genetic analysis. One goal is to identify the phenotypic effects of elevated temperatures and other stresses on Arabidopsis plants null for Hsp21. An Hsp21 null mutant line was identified in which a point mutation in the conserved intron base at the 3' splice site prevents the accumulation of Hsp21 after heat stress. Mutants unable to synthesize Hsp21 during stress showed a mild heat-sensitive phenotype. Additional assays to study chlorophyll levels and the effects of oxidative stress will be performed. Another goal is to identify possible in vivo substrates of Hsp21. This is being approached by introducing an affinity tag (strep-tag II encoding WSHPQFEK) to the 3' end of the Hsp21 gene. The DNA encoding Hsp21-strep has been inserted into an entry vector and will be recombined with a plant transformation plasmid, which is transformed into Agrobacterium tumefaciens. This bacterium is used to insert the tagged protein gene into plants null for Hsp21. Hsp21 and any associated proteins can then be isolated by separating cell lysates from these plants via streptactin affinity chromatography. Mass spectrometry will be used to determine the identity of the in vivo substrates of Hsp21. It is hypothesized that heat-labile proteins crucial for chloroplast function are most likely to be protected by Hsp21.
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Almeida, Breno Fernando Martins de. "O papel da heme oxigenase-1 na leishmaniose visceral canina /". Araçatuba, 2016. http://hdl.handle.net/11449/143430.

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Orientador: Valéria Marçal Felix de Lima
Coorientador: Paulo César Ciarlini
Banca:Luiz Daniel de Barros
Banca:Flavia Lombardi Lopes
Banca:Suely Regina Mogami Bomfim
Banca; Rosimeri de Oliveira Vasconcelos
Resumo: A leishmaniose visceral canina (LVC) é uma doença crônica que causa imunossupressão nos animais doentes, principalmente por prejudicar a resposta imunológica celular, diminuindo a proliferação linfocitária e a capacidade fagocítica das células de defesa. Recentemente, a enzima heme oxigenase-1 (HO-1) vem ganhando destaque por estar envolvida na regulação da resposta imune celular em algumas condições patológicas, sendo uma enzima induzível por condições de estresse, como o estresse oxidativo que sabidamente ocorre na LVC. Nesse contexto, esse trabalho teve por objetivo determinar o papel da HO-1 na LVC, determinando sua concentração e expressão em cães infectados e saudáveis, correlacionando-a com o estresse oxidativo, carga parasitária e IL-10. Objetivou-se também avaliar o efeito da indução e inibição da enzima sobre a resposta linfoproliferativa de células de linfonodo de cães doentes e sobre a taxa de infecção macrofágica por promastigotas de Leishmania infantum, determinando as citocinas envolvidas. Os cães com LVC apresentaram marcante estresse oxidativo e aumento da concentração e expressão de HO-1, obtendo-se correlação positiva entre HO-1e estresse oxidativo e IL-10 de acordo com o tecido analisado. A inibição de HO-1 aumentou a taxa de proliferação celular na presença de antígeno solúvel de L. infantum, enquanto a indução de HO-1 diminuiu a taxa de proliferação antígeno-específica e aumentou a taxa de infecção macrofágica e o número de amastigotas por macrófago. Con... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Canine visceral leishmaniasis (CVL) is a chronic disease that causes immunosuppression by reducing the cellular response of infected animals, impairing the cell proliferation and the phagocytic ability of defense cells. Recently, heme oxygenase-1 (HO-1) has been highlighted for being involved in regulation of cell response in certain pathological conditions, and for being an enzyme that can be induced by stress conditions, such as oxidative stress, that is known to occur in CVL. In this context, this study aimed to determine the role of HO-1 in CVL, determining its levels and expression in infected and healthy dogs, correlating these findings with oxidative stress, parasite load and IL-10. The effect of induction and inhibition of HO-1 on lymphoproliferative response by lymph node cells of infected dogs and macrophage infection rate by promastigotes of Leishmania infantum were also evaluated. Dogs with CVL showed marked oxidative stress and increased levels and expression of HO-1, obtaining a positive correlation between HO-1 and oxidative stress and IL-10 in a tissue-dependent way. Inhibition of HO-1 increased proliferation rate in the presence of L. infantum soluble antigen, while induction of HO-1 decreased antigen-specific proliferation and increased macrophage infection rate and number of amastigotes per macrophage. The increase in HO-1 metabolism observed in CVL is associated to oxidative stress present in these dogs and could be one of the mechanisms involved in the in... (Complete abstract click electronic access below)
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Gibert, Benjamin. "La protéine de stress Hsp27 / HspB1, une cible de choix en thérapie anti-cancéreuse". Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00733751.

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Hsp27 appartient à la famille des protéines dites de survie comme Bcl2 ou la survivine. C'est une protéine anti-apoptotique qui subit une dérégulation de son expression dans de nombreux types tumoraux. Elle est caractérisée comme étant une cible thérapeutique majeure. Au cours de ma thèse, j'ai isolé des peptides stabilisés, dit aptamères, capables d'inhiber fonctionnellement les activités anti-apoptotiques et tumorigènes d'Hsp27. Ces aptamères perturbent la biochimie structurale de Hsp27 et induisent le blocage du cycle cellulaire in vivo. Parallèlement à cette étude, j'ai caractérisé les effets de la déplétion de Hsp27 sur la formation de métastases et de tumeurs osseuses. J'ai aussi montré que la modification du taux de Hsp27 induisait la dégradation de différentes protéines, dites clientes, comme la caspase3, HDAC6 et STAT2.
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Książki na temat "Hsp31"

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Public District School Board Writing Partnership (Ontario) i Ontario Ministry of Education, red. Introduction to anthropology, psychology, and sociology: Course profile, grade 11, university/college preparation HSP3M. [Ontario]: Queen's Printer for Ontario, 2001.

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Esquisse de cours 11e année: Introduction à la psychologie, à la sociologie et à l'anthropologie hsp3m cours préuniversitaire. Vanier, Ont: CFORP, 2001.

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Części książek na temat "Hsp31"

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Arrigo, André Patrick. "HspB1". W Encyclopedia of Signaling Molecules, 2451–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101690.

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Arrigo, André Patrick. "HspB1". W Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101690-1.

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Iwamoto, Ryo, Eisuke Mekada, Thomas G. Hofmann, Eva Krieghoff-Henning, Masaaki Kobayashi, Ken Takamatsu, Jennifer Defren i in. "Hspb1-Kinase". W Encyclopedia of Signaling Molecules, 886. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100627.

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Arrigo, André-Patrick. "Structure–Functions of HspB1 (Hsp27)". W Methods in Molecular Biology, 105–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-295-3_9.

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Benndorf, Rainer, i Peter R. Jungblut. "Reconsidering Old Data: Non-canonical HspB1 Species and the Enigma of the Cytoskeletal Function of HspB1". W Heat Shock Proteins, 471–85. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16077-1_20.

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Panneerselvam, Lakshmikanthan, Azhwar Raghunath, Kiruthika Sundarraj i Ekambaram Perumal. "HO-1/HSP32 and Cardiac Stress Signaling". W Heat Shock Proteins, 139–59. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03952-3_8.

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Doshi, Bindi M., Lawrence E. Hightower i Juliet Lee. "Heat Shock Alters Keratocyte Movement and Morphology: Exploring a Role for HSP27 (HSPB1)". W Heat Shock Proteins, 457–69. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16077-1_19.

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Arrigo, André-Patrick. "Analysis of HspB1 (Hsp27) Oligomerization and Phosphorylation Patterns and Its Interaction with Specific Client Polypeptides". W Methods in Molecular Biology, 163–78. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7477-1_12.

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Musiani, Daniele, John David Konda, Simona Pavan, Erica Torchiaro, Jessica Erriquez, Martina Olivero i Maria Flavia Di Renzo. "Heat Shock Protein 27 (HSP27, HSPB1) Is Up-Regulated by Targeted Agents and Confers Resistance to Both Targeted Drugs and Chemotherapeutics". W Heat Shock Proteins, 17–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17211-8_2.

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Arrigo, Andre-Patrick. "Anti-apoptotic, Tumorigenic and Metastatic Potential of Hsp27 (HspB1) and αB-crystallin (HspB5): Emerging Targets for the Development of New Anti-Cancer Therapeutic Strategies". W Heat Shock Proteins in Cancer, 73–92. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6401-2_4.

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Streszczenia konferencji na temat "Hsp31"

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Song, Yan, Yi-ling Hou, Wan-ru Hou, Guang-fu Wu i Tian Zhang. "cDNA, Genomic Sequence Cloning and Sequence Analysis of Heat Shock Protein Beta-1 Gene (HSPB1) from the Giant Panda (Ailuropoda melanoleuca)". W 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5517383.

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Raporty organizacyjne na temat "Hsp31"

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McElwain, Terry F., Eugene Pipano, Guy H. Palmer, Varda Shkap, Stephn A. Hines i Wendy C. Brown. Protection of Cattle against Babesiosis: Immunization against Babesia bovis with an Optimized RAP-1/Apical Complex Construct. United States Department of Agriculture, wrzesień 1999. http://dx.doi.org/10.32747/1999.7573063.bard.

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Previous research and current efforts at control of babesiosis fall short of meeting the needs of countries where the disease is endemic, such as Israel, as well as the needs of exporting countries and countries bordering on endemic areas, such as the U.S. Our long-term goal is to develop improved methods of immunization against bovine babesiosis based on an understanding of the molecular mechanisms of immune protection and parasite targets of a protective immune response. In our previous BARD project, we established the basis for focusing on rhoptry antigens as components of a subunit vaccine against bovine babesiosis, and for additional research to better characterize rhoptry associated protein-1 (RAP-1) as a target of protective immunity. In this continuation BARD project, our objectives were to [1] optimize the immune response against RAP-1, and [2] identify additional rhoptry candidate vaccine antigens. The entire locus encoding B. bovis RAP-1 was sequenced, and the rap-1 open reading frame compared among several strains. Unlike B. bigemina, in which multiple gene copies with variant domains encode RAP-1, the B. bovis RAP-1 locus contains only two identical genes which are conserved among strains. Through testing of multiple truncated constructs of rRAP-1, one or more immunodominant T cell epitopes were mapped to the amino terminal half of RAP-1. At least one linear and one conformational B cell epitope have been demonstrated in the same amino terminal construct, which in B. bigemina RAP-1 also contains an epitope recognized by neutralizing antibody. The amine terminal half of the molecule represents the most highly conserved part of the gene family and contains motifs conserved broadly among the apicomplexa. In contrast, the carboxy terminal half of B. bovis RAP-1 is less well conserved and contains multiple repeats encoding a linear B cell epitope potentially capable of inducing an ineffective, T cell independent, type 2 immune response. Therefore, we are testing an amino terminal fragment of RAP-1 (RAP-1N) in an immunization trial in cattle. Cattle have beer immunized with RAP-1N or control antigen, and IL-12 with Ribi adjuvant. Evaluation of the immune response is ongoing, and challenge with virulent B. bovis will occur in the near future. While no new rhoptry antigens were identified, our studies did identify and characterize a new spherical body antigen (SBP3), and several heat shock proteins (HSP's). The SBP3 and HSP21 antigens stimulate T cells from immune cattle and are considered new vaccine candidates worthy of further testing. Overall, we conclude that a single RAP-1 vaccine construct representing the conserved amino terminal region of the molecule should be sufficient for immunization against all strains of B. bovis. While results of the ongoing immunization trial will direct our next research steps, results at this time are consistent with our long term goal of designing a subunit vaccine which contains only the epitopes relevant to induction of protective immunity. Parallel studies are defining the mechanisms of protective immunity. Apicomplexan protozoa, including babesiosis and malaria, cause persistent diseases for which control is inadequate. The apical organelles are defining features of these complex protozoa, and have been conserved through the evolutionary process, Past and current BARD projects on babesiosis have established the validity and potential of exploiting these conserved organelles in developing improved control methods applicable to all apicomplexan diseases.
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