Genomics

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Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis


ABSTRACT: Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis

PROVIDER: PRJNA606600 | ENA |

REPOSITORIES: ENA

Dataset's files

Source:
Action DRS
SRR11085314.fastq.gz Fastqsanger.gz
SRR11085315.fastq.gz Fastqsanger.gz
SRR11085316.fastq.gz Fastqsanger.gz
SRR11085317.fastq.gz Fastqsanger.gz
SRR11085318.fastq.gz Fastqsanger.gz
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Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis.

Riching Andrew S AS   Danis Etienne E   Zhao Yuanbiao Y   Cao Yingqiong Y   Chi Congwu C   Bagchi Rushita A RA   Klein Brianna J BJ   Xu Hongyan H   Kutateladze Tatiana G TG   McKinsey Timothy A TA   Buttrick Peter M PM   Song Kunhua K  

Journal of molecular and cellular cardiology 20201224


Direct reprogramming of fibroblasts into cardiomyocytes (CMs) represents a promising strategy to regenerate CMs lost after ischemic heart injury. Overexpression of GATA4, HAND2, MEF2C, TBX5, miR-1, and miR-133 (GHMT2m) along with transforming growth factor beta (TGF-β) inhibition efficiently promote reprogramming. However, the mechanisms by which TGF-β blockade promotes cardiac reprogramming remain unknown. Here, we identify interactions between the histone H3 lysine 27 trimethylation (H3K27me3)  ...[more]

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