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首页> 外文期刊>The FEBS journal >p53 mediated regulation of coactivator associated arginine methyltransferase 1 (CARM1) expression is critical for suppression of adipogenesis
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p53 mediated regulation of coactivator associated arginine methyltransferase 1 (CARM1) expression is critical for suppression of adipogenesis

机译：P53介导的调节剂的调节相关的精氨酸甲基转移酶1（CARM1）表达对于抑制脂肪发生至关重要

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摘要

Coactivator‐associated arginine methyltransferase 1 (CARM1/PRMT4) is a type I arginine methyltransferase that mediates transcriptional activation via methylation of histone H3 on R17, R26, and R42. CARM1 is also a coactivator of transcription of various transcription factors such as NF‐kB, MEF2C, β‐catenin, p53, PPAR‐gamma etc. CARM1 has been functionally implicated in maintenance of pluripotency, cellular differentiation, and tumorigenesis; where its expression status plays an important role. Although its expression has been shown to be regulated by a few miRNAs in different contexts at post‐transcriptional level, transcriptional regulation of CARM1 gene is still unexplored. In this report we demonstrate that CARM1 is a p53 responsive gene, where p53 could suppress CARM1 promoter‐driven luciferase expression. CARM1 gene expression was found to be repressed by p53 in 3T3L1 preadipocytes when activated with Nutlin‐3a treatment. Ectopic overexpression of CARM1 could rescue inhibitory effect of p53 on adipogenesis, suggesting a role of p53‐CARM1 axis of regulation operational in the context of adipocyte differentiation. p53 and CARM1 showed antagonistic regulatory influence on PPAR‐gamma expression; which suggests that p53‐mediated suppression of adipogenesis could be partly via repression of CARM1 expression. Taken together these observations provide convincing mechanistic explanation for p53 function in the context of adipocyte differentiation process.
机译：共粘膜相关的精氨酸甲基转移酶1（CARM1 / PRMT4）是I型精氨酸甲基转移酶，其在R17，R26和R42上通过组蛋白H3的甲基化介导转录活化。 CARM1也是诸如NF-KB，MEF2C，β-Catenin，P53，PPAR-GAMMA等的各种转录因子的转录的共觉器。CARM1已经在功能上涉及维持多能性，细胞分化和肿瘤鉴定;它的表达式状态扮演重要角色。虽然其表达已被在转录后水平的不同环境中由几种miRNA调节，但Carm1基因的转录调节仍未探明。在本报告中，我们证明CARM1是P53响应基因，其中P53可以抑制CARM1启动子驱动的荧光素酶表达。发现CARM1基因表达在用Nutlin-3a处理中激活时，在3T3L1前脂肪细胞中被P53抑制。 CARM1的异位过表达可以拯救P53对脂肪生成的抑制作用，这表明在脂肪细胞分化的背景下的P53-CARM1调节轴的作用。 P53和CARM1对PPAR-GAMMA表达表现出对拮抗性调节影响;这表明P53介导的抑制脂肪发生可以部分通过抑制CARM1表达。在脂肪细胞分化过程的背景下，这些观察结果提供了对P53功能的令人信服的机制解释。

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