ATF4-dependent transcription mediates signaling of amino acid limitation

被引：518

作者：

Kilberg, Michael S. ^{[1
]}

Shan, Jixiu ^{[1
]}

Su, Nan ^{[1
]}

机构：

[1] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2009年 / 20卷 / 09期

基金：

美国国家卫生研究院;

关键词：

ASPARAGINE SYNTHETASE GENE; DIETARY-PROTEIN RESTRICTION; MESSENGER-RNA STABILIZATION; INTEGRATED STRESS-RESPONSE; HUMAN HEPATOMA-CELLS; TRANSPORT SYSTEM-A; TRANSLATIONAL CONTROL; ENDOPLASMIC-RETICULUM; HEPG2; CELLS; ADAPTIVE REGULATION;

D O I：

10.1016/j.tem.2009.05.008

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Mammals respond to dietary nutrient fluctuations; for example, deficiency of dietary protein or an imbalance of essential amino acids activates an amino acid response (AAR) signal transduction pathway, consisting of detection of uncharged tRNA by the GCN2 kinase, elF2 alpha phosphorylation and ATF4 expression. In concert with heterodimerization partners, ATF4 activates specific genes via a CCAAT-enhancer binding protein-activating transcription factor response element (CARE). This review outlines the ATF4-dependent transcriptional mechanisms associated with the AAR, focusing on progress during the past 5 years. Recent evidence suggests that maternal nutrient deprivation not only has immediate metabolic effects on the fetus, but also triggers gene expression changes in adulthood, possibly through epigenetic mechanisms. Therefore, understanding the transcriptional programs initiated by amino acid limitation is crucial and timely.

引用

页码：436 / 443

页数：8

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