p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling.

By A. Budanov, M. Karin. Cell, 2008

1,340 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/24547df20ab0ce061dfec91e3b73899e1e645e28

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In Molecular Biology

Citations in the corpus

Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “Many products of these target genes, such as AMP-activated protein kinase, tuberous sclerosis protein 2, and sestrin1/2 converge on the mTOR pathway.(80,81) mTOR is a negative regulator of autophagy, and inhibition of this pathway results in the induction of autophagy.”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “to negatively regulate the kinase mTOR (mammalian target of rapamycin), a central node in the control of protein synthesis (Budanov and Karin, 2008; Feng et al., 2007a) (Figure 1).”
LKB1 and AMPK control of mTOR signalling and growth (2009, background): “Recently, the critical transcriptional targets of p53 that mediate the suppression of mTORC1 were identified as Sestrin1 and Sestrin2 (Budanov & Karin 2008).”
Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “The p53 target genes Sestrin1 and Sestrin2 phosphorylate and activate AMPK and promote autophagy.(178) p53 induces mitophagy by increasing the level of BNIP3.”
Regulation of mTORC1 by amino acids (2014, neutral): “The TSC complex, whose loss underlies a hamartomatous syndrome of the same name (17, 18), serves as a central hub for numerous extracellular and intracellular inputs including mitogen and growth factor signaling (19-23), energy levels (24), oxygen availability (25, 26) and genotoxic stress (27), whi”
Translational regulation of gene expression during conditions of cell stress. (2010, background): “Signaling to mTOR, and thus 4EBP1, upon DNA damage appears to occur through a p53-dependent pathway requiring transcriptional activation of Sestrin1 and Sestrin2, which in turn activate AMP-responsive protein kinase (AMPK), which then activates the repressor of mTOR TSC2 (Budanov and Karin, 2008).”
Nutrient sensing and TOR signaling in yeast and mammals (2017, positive): “…proposed to repress mTORC1 through at least three different mechanisms: (i) by activating AMPK (AMP-activated protein kinase) and the TSC complex (Budanov & Karin, 2008), (ii) by acting as a GDI (guanosine dissociation inhibitor) to prevent GDP dissociation from RAGA/B (Peng et al , 2014), and…”
The LKB1-AMPK pathway: metabolism and growth control in tumor suppression (2009, background): “43 , and this led to the discovery of sestrin 1 ( SESN1 ) and sestrin 2 ( SESN2 ) — p53 target genes that inhibit mTOR signallin”
ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010, background): “The p53-regulated genes Sestrin 1 and Sestrin 2 were shown to activate AMPK and repress mTORC1 signaling in response to camptothecin-induced genotoxic stress in a redoxindependent manner (21).”