Extended self-renewal and accelerated reprogramming in the absence of Kdm5b

ChEBI2013-10-14 更新2026-07-21 收录

干细胞重编程

表观遗传调控

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-46893 数据链接链接失效反馈

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Extended self-renewal and accelerated reprogramming in the absence of Kdm5b

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2013-10-14

Depletion of H3K36me2 recapitulates epigenomic and phenotypic changes induced by the H3.3K36M oncohistone mutation

组蛋白修饰与肿瘤发生

表观遗传调控

In this study, our results support a functional divergence between H3K36me2 and H3K36me3 and their non-redundant roles in H3K36M-driven oncogenesis Overall design: 17 ChIP-seq samples, 3 RNA-seq sampl

NIAID Data Ecosystem50

A prion accelerates proliferation at the expense of lifespan

朊病毒与细胞衰老

表观遗传调控

Organisms often commit to one of two strategies: living fast and dying young or living slow and dying old. In fluctuating environments, however, switching between these two strategies could be advanta

Alliance of Genome Resources00

Addressing the specific roles of histone modifications in transcriptional repression [RNA-seq]

组蛋白修饰转录抑制

表观遗传调控

Our understanding of epigenetic processes is based on the hypothesis that individual posttranslational modifications of DNA and histones, or combinations thereof, function to direct unique downstream

NIAID Data Ecosystem00

Identification of introduced and stably inherited DNA methylation variants in soybean associated with soybean cyst nematode parasitism [RNA-seq]

大豆抗线虫研究

表观遗传调控

Methylome changes mediated by the soybean cyst nematode resistance gene GmSHMT08 Overall design: Examining the changes in the transcriptome of two nearly isogenic lines (TN09-16 and TN09-29) under soy

NIAID Data Ecosystem10

DNMT3A Reads and Connects Histone H3K36me2 to DNA methylation [RNA-seq]

表观遗传调控

甲基化反应机制

DNA methylation at the 5-position of cytosine (5mC) is a crucial epigenetic mark in regulating biological processes including gene silencing, gene imprinting, and X chromosome inactivation. It has lon

NIAID Data Ecosystem00

Extended self-renewal and accelerated reprogramming in the absence of Kdm5b

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