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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome wide mapping of H3K27me3 in differentiated mouse podocytes

ABSTRACT: We explored H3K27me3 binding sites in the genome of differentiated, conditionally immortalized mouse podocytes. Cells were allowed to differentiate for 14 days, following thermoshifting, before treatment with either vehicle (DMSO) or the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanocin A (DZNep, 5ÂµM for 48 hours) which degrades the histone methyltransferase, EZH2 ordinarily responsible for H3K27 trimethylation (H3K27me3). DNA was immunopreciptated with an H3K27me3-specific antibody. Studying H3K27me3 modification in Mouse Podocyte

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Advani

PROVIDER: E-GEOD-69610 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Histone Methyltransferase Enzyme Enhancer of Zeste Homolog 2 Protects against Podocyte Oxidative Stress and Renal Injury in Diabetes.

Siddiqi Ferhan S FS Majumder Syamantak S Thai Kerri K Abdalla Moustafa M Hu Pingzhao P Advani Suzanne L SL White Kathryn E KE Bowskill Bridgit B BB Guarna Giuliana G Dos Santos Claudia C CC Connelly Kim A KA Advani Andrew A

Journal of the American Society of Nephrology : JASN 20151103 7

Epigenetic regulation of oxidative stress is emerging as a critical mediator of diabetic nephropathy. In diabetes, oxidative damage occurs when there is an imbalance between reactive oxygen species generation and enzymatic antioxidant repair. Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (T ...[more]

PMID: 26534922

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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