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Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment

dc.contributor.authorSingh, Sandeep
dc.contributor.authorRaina, Varsheish
dc.contributor.authorChavali, Pavithra Lakshminarsimhan
dc.contributor.authorDubash, Taronish
dc.contributor.authorKadreppa, Sreenath
dc.contributor.authorParab, Pradeep
dc.contributor.authorChattopadhyay, Samit
dc.date.accessioned2018-07-14T01:19:07Z
dc.date.available2018-07-14T01:19:07Z
dc.date.issued2012
dc.identifier.citationSingh, S., Raina, V., Chavali, P. L., Dubash, T., Kadreppa, S., Parab, P., & Chattopadhyay, S. (2012). Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment. Bmc Molecular Biology, 13. doi: 10.1186/1471-2199-13-28en_US
dc.identifier.issn14712199
dc.identifier.urihttp://kr.cup.edu.in/handle/32116/1447
dc.description.abstractBackground: GAD65 (Glutamic acid decarboxylase 65 KDa isoform) is one of the most important auto-antigens involved in Type 1 diabetes induction. Although it serves as one of the first injury markers of ?-islets, the mechanisms governing GAD65 expression remain poorly understood. Since the regulation of GAD65 is crucial for the proper functioning of insulin secreting cells, we investigated the stress induced regulation of GAD65 transcription.Results: The present study shows that SMAR1 regulates GAD65 expression at the transcription level. Using a novel protein-DNA pull-down assay, we show that SMAR1 binding is very specific to GAD65 promoter but not to the other isoform, GAD67. We show that Streptozotocin (STZ) mediated DNA damage leads to upregulation of SMAR1 and p53 expression, resulting in elevated levels of GAD65, in both cell lines as well as mouse ?-islets. SMAR1 and p53 act synergistically to up-regulate GAD65 expression upon STZ treatment.Conclusion: We propose a novel mechanism of GAD65 regulation by synergistic activities of SMAR1 and p53. ? 2012 Singh et al.; licensee BioMed Central Ltd.en_US
dc.language.isoen_USen_US
dc.subjectGlutamate Decarboxylase 65en_US
dc.subjectGlutamate Decarboxylase 67en_US
dc.subjectProtein P53en_US
dc.subjectSmar1 Proteinen_US
dc.subjectStreptozocinen_US
dc.subjectTumor Suppressor Proteinen_US
dc.subjectUnclassified Drugen_US
dc.subjectAnimal Cellen_US
dc.subjectCell Cultureen_US
dc.subjectDna Damageen_US
dc.subjectGene Expressionen_US
dc.subjectGene Expression Regulationen_US
dc.subjectHumanen_US
dc.subjectHuman Cellen_US
dc.subjectIn Vitro Studyen_US
dc.subjectMouseen_US
dc.subjectNonhumanen_US
dc.subjectPancreas Islet Beta Cellen_US
dc.subjectProtein Bindingen_US
dc.subjectUpregulationen_US
dc.subjectAnimalsen_US
dc.subjectBase Sequenceen_US
dc.subjectCell Cycle Proteinsen_US
dc.subjectCell Lineen_US
dc.subjectChromatin Immunoprecipitationen_US
dc.subjectDnaen_US
dc.subjectDna Damageen_US
dc.subjectDna Primersen_US
dc.subjectDna-Binding Proteinsen_US
dc.subjectElectrophoreticen_US
dc.titleRegulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatmenten_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1471-2199-13-28
dc.identifier.urlhttps://bmcmolbiol.biomedcentral.com/articles/10.1186/1471-2199-13-28
dc.title.journalBMC Molecular Biology


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