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Does Smad6 methylation control BMP signaling in cancer?

机译:Smad6甲基化可控制癌症中的BMP信号传导吗?

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摘要

Bone morphogenetic proteins (BMPs), a class of secreted TGF-beta-related proteins, play key roles in many cell differentiation decisions in metazoan development. BMP signaling is dysregulated in developmental syndromes and contributes to progressive diseases, including cancers. BMP ligands activate signaling responses through tetrameric complexes consisting of 2 type II (RII) and 2 type I (RI) transmembrane receptor kinases. Ligand binding induces RII receptors to phosphorylate and activate RI receptors, and these then activate the intracellu-lar effectors Smad1 and Smad5 through C-terminal serine phosphorylation, which stands in contrast to activation of Smad2 and Smad3 by TGF-betas and activins.
机译:骨形态发生蛋白(BMP)是一类与TGF-β相关的分泌蛋白,在后生动物发育的许多细胞分化决定中起着关键作用。 BMP信号在发育综合征中失调,并导致包括癌症在内的进行性疾病。 BMP配体通过由2种II型(RII)和2种I型(RI)跨膜受体激酶组成的四聚体复合物激活信号传导反应。配体结合诱导RII受体磷酸化并激活RI受体,然后这些受体通过C端丝氨酸磷酸化激活细胞内效应子Smad1和Smad5,这与TGF-betas和激活素激活Smad2和Smad3相反。

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