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Please use this identifier to cite or link to this item: http://dspace.bits-pilani.ac.in:8080/jspui/handle/123456789/15359
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dc.contributor.authorMajumder, Syamantak-
dc.contributor.authorChowdhury, Shibasish-
dc.date.accessioned2024-08-22T10:37:15Z-
dc.date.available2024-08-22T10:37:15Z-
dc.date.issued2023-05-
dc.identifier.uriURL-
dc.identifier.urihttps://www.biorxiv.org/content/10.1101/2023.05.12.540614v2-
dc.identifier.urihttp://dspace.bits-pilani.ac.in:8080/jspui/xmlui/handle/123456789/15359-
dc.description.abstractEndothelial senescence has been linked to several cardiovascular diseases. Dysregulation of proteins of the shelterin complex including TRF2 and TERF2IP causes senescence as it hampers DNA repair and cell proliferation. However, whether exposure to hyperglycemia interplays with proteins of the shelterin complex thus further dictates the senescent phenotype of endothelial cells (EC) remain to be explored.en_US
dc.language.isoenen_US
dc.subjectBiologyen_US
dc.subjectTERF2IPen_US
dc.titleRegulation of shelterin proteins TERF2IP and TRF2 by H3K4me3-p65 axis drives hyperglycemia dependent endothelial senescenceen_US
dc.typePlan or blueprinten_US
Appears in Collections:Department of Biological Sciences

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