Smyd3는 Cancer development와 관련된 protein methyltransferase. 쥐에서의 Smyd3 발현은 liver, 화학적으로 유도된 colon cancer formation을 필요로 한다. 이들 기관에서 Cell proliferation, EMT, AK-STAT signaling pathway와 관련된 핵심 조절자들의 전사를 촉진한다.

Smyd3은 H3K4Me3-modified histone tail과 상호작용하여 대부분 유전자의 활성을 촉진한다.

타겟 유전자에 대한 Smyd3 binding density는 RNA pol2 density와 상관관계가 있다.

2016-05-14 원희영 저널 발표

Summary #

Introduction #

Results #

Smyd3 Inactivation Protects against Chemically Induced HCC and CRC Development #

Smyd3 Is Dispensable for Carcinogen-Induced Cell Death and Inflammation, but Is Required for Compensatory Cell Proliferation #

Smyd3 Regulates Oncogene Activation and Epithelial to Mesenchymal Transition #

Smyd3 Potentiates the RNA Pol-II-Mediated Transcription of Cancer-Promoting Genes #

The Mechanism of Target Gene Selection by Smyd3 Involves Interaction with Trimethylated H3K4 Tails #

Discussion #

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