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ATF4 MTOR (1 - 3 of 3)
PMID: 17430894
Role of the transcription factor ATF4 in the anabolic actions of insulin and the anti-anabolic actions of glucocorticoids.
... of ATF4 required the mammalian target of rapamycin complex ...   (details)

ATF4 MTOR

Type:  positive regulation
Is this interaction correct?
Yes
No

Comments

PMID: 17430894

Role of the transcription factor ATF4 in the anabolic actions of insulin and the anti-anabolic actions of glucocorticoids.
Source

The Journal of biological chemistry (6/8/2007)

Abstract

Role of the transcription factor ATF4 in the anabolic actions of insulin and the anti-anabolic actions of glucocorticoids. In most mammalian cells, insulin and glucocorticoids promote anabolism and catabolism, respectively. Whereas the opposing effects of insulin and glucocorticoids on catabolic gene expression have been explained at the molecular level, comparatively little is known about how these hormones alter anabolic gene expression. These studies identify ATF4 as an anabolic transcription factor that is repressed by glucocorticoids and induced by insulin. Insulin-mediated induction of ATF4 required the mammalian target of rapamycin complex 1, was required for the activation of a genetic program for the cellular uptake of essential amino acids and the synthesis of nonessential amino acids and aminoacyl-tRNAs, and was coupled to the repression of Foxo-dependent genes needed for protein and lipid catabolism. These results suggest that ATF4 plays a central role in hormonal regulation of amino acid and protein anabolism by coupling amino acid uptake and synthesis, as well as the generation of charged tRNAs, to mammalian target of rapamycin complex 1-mediated mRNA translation.

PMID: 19439225
Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress.
Activating transcription factor 4 and ... negatively regulate the mammalian target of rapamycin via ...   (details)

ATF4 MTOR

Type:  positive regulation
Is this interaction correct?
Yes
No

Comments

PMID: 19439225

Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress.
Source

Free radical biology & medicine (4/15/2009)

Abstract

Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress. Regulation of mRNA translation in mammalian cells involves the coordinated control of mammalian target of rapamycin (mTOR) signaling. At present, limited information is available on the potential relevance of mTOR regulation, although translation inhibition during oxidative and endoplasmic reticulum (ER) stress is clearly important. In this study, we show that activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-beta (C/EBP-beta) negatively regulate mTOR via Redd1 expression in response to oxidative and ER stress. Oxidative and ER stress conditions induce rapid and significant activation of ATF4 downstream of eIF2alpha phosphorylation, which is responsible for Redd1 expression. In our experiment, overexpression of ATF4 was associated with reduced mTOR activity via Redd1 expression, whereas suppression of ATF4 levels with small interfering RNA led to the recovery of decreased mTOR activity mediated by downregulation of Redd1 during oxidative and ER stress. We additionally identified Redd1 as a downstream effector of C/EBP-beta stimulated by ATF4 activated under the stress conditions examined. RNA interference studies provided further evidence of the requirement of C/EBP-beta for Redd1 expression. We conclude that the Redd1 gene is transactivated by the ATF4 and C/EBP family of transcription factors, leading to mTOR inhibition in response to oxidative and ER stress.

... that activating transcription factor 4 (ATF4) and ... negatively regulate mTOR via ...   (details)

ATF4 MTOR

Type:  positive regulation
Is this interaction correct?
Yes
No

Comments

PMID: 19439225

Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress.
Source

Free radical biology & medicine (4/15/2009)

Abstract

Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress. Regulation of mRNA translation in mammalian cells involves the coordinated control of mammalian target of rapamycin (mTOR) signaling. At present, limited information is available on the potential relevance of mTOR regulation, although translation inhibition during oxidative and endoplasmic reticulum (ER) stress is clearly important. In this study, we show that activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-beta (C/EBP-beta) negatively regulate mTOR via Redd1 expression in response to oxidative and ER stress. Oxidative and ER stress conditions induce rapid and significant activation of ATF4 downstream of eIF2alpha phosphorylation, which is responsible for Redd1 expression. In our experiment, overexpression of ATF4 was associated with reduced mTOR activity via Redd1 expression, whereas suppression of ATF4 levels with small interfering RNA led to the recovery of decreased mTOR activity mediated by downregulation of Redd1 during oxidative and ER stress. We additionally identified Redd1 as a downstream effector of C/EBP-beta stimulated by ATF4 activated under the stress conditions examined. RNA interference studies provided further evidence of the requirement of C/EBP-beta for Redd1 expression. We conclude that the Redd1 gene is transactivated by the ATF4 and C/EBP family of transcription factors, leading to mTOR inhibition in response to oxidative and ER stress.