2010
DOI: 10.1128/mcb.00688-09
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A Role for p38 Stress-Activated Protein Kinase in Regulation of Cell Growth via TORC1

Abstract: The target of rapamycin (TOR) complex 1 (TORC1) signaling pathway is a critical regulator of translation and cell growth. To identify novel components of this pathway, we performed a kinome-wide RNA interference (RNAi) screen in Drosophila melanogaster S2 cells. RNAi targeting components of the p38 stress-activated kinase cascade prevented the cell size increase elicited by depletion of the TOR negative regulator TSC2. In mammalian and Drosophila tissue culture, as well as in Drosophila ovaries ex vivo, p38-ac… Show more

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Cited by 81 publications
(95 citation statements)
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“…The correlations between FTI, FAK and p38 may represent a single pathway, as a hypertrophic signaling pathway involving integrin-FAK and p38 induced by mechanical stress has been reported (Aikawa et al, 2002;Lal et al, 2007). Activation of p38 may contribute to increased protein synthesis via phosphorylation of TSC2-and MNK-induced phosphorylation of eIF4E and p70S6k on T421/S424 (Cully et al, 2010;Hernández et al, 2011;Wang et al, 1998) and is required for myogenic differentiation via activation of MEF2 and MRF4 (Lluís et al, 2006), both processes required for muscle hypertrophy. The correlation found between p38 and mTOR in both experiments is consistent with the observations in Drosophila that p38 is a positive regulator of mTOR through TSC1/2-dependent mechanisms (Cully et al, 2010), potentially by promoting interaction of TSC1/2 and 14-3-3 (Hernández et al, 2011).…”
Section: Mechanical Activation Of a P38-mtor Axismentioning
confidence: 95%
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“…The correlations between FTI, FAK and p38 may represent a single pathway, as a hypertrophic signaling pathway involving integrin-FAK and p38 induced by mechanical stress has been reported (Aikawa et al, 2002;Lal et al, 2007). Activation of p38 may contribute to increased protein synthesis via phosphorylation of TSC2-and MNK-induced phosphorylation of eIF4E and p70S6k on T421/S424 (Cully et al, 2010;Hernández et al, 2011;Wang et al, 1998) and is required for myogenic differentiation via activation of MEF2 and MRF4 (Lluís et al, 2006), both processes required for muscle hypertrophy. The correlation found between p38 and mTOR in both experiments is consistent with the observations in Drosophila that p38 is a positive regulator of mTOR through TSC1/2-dependent mechanisms (Cully et al, 2010), potentially by promoting interaction of TSC1/2 and 14-3-3 (Hernández et al, 2011).…”
Section: Mechanical Activation Of a P38-mtor Axismentioning
confidence: 95%
“…Activation of p38 may contribute to increased protein synthesis via phosphorylation of TSC2-and MNK-induced phosphorylation of eIF4E and p70S6k on T421/S424 (Cully et al, 2010;Hernández et al, 2011;Wang et al, 1998) and is required for myogenic differentiation via activation of MEF2 and MRF4 (Lluís et al, 2006), both processes required for muscle hypertrophy. The correlation found between p38 and mTOR in both experiments is consistent with the observations in Drosophila that p38 is a positive regulator of mTOR through TSC1/2-dependent mechanisms (Cully et al, 2010), potentially by promoting interaction of TSC1/2 and 14-3-3 (Hernández et al, 2011). The persistence of the p38-mTOR module even under high metabolic stress in the HDC protocols suggests that activation of a force-related growth pathway can occur simultaneous with activation of AMPK.…”
Section: Mechanical Activation Of a P38-mtor Axismentioning
confidence: 99%
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“…The p38 pathway belongs to a MAPK signaling module, a highly conserved pathway known for its role in stress responses, including those to pro-inflammatory cytokines and UV irradiation as well as heat and osmotic shock [9]. There is a body of evidence showing crosstalk between the p38 and the mTORC1 pathways [10,11]. The role of the p38 pathway in global stress responses prompted Zheng and colleagues to investigate whether p38 regulates mTORC1, following an energy deprivation episode.…”
mentioning
confidence: 99%
“…In Drosophila, three p38-MAPK-encoding genes, p38a (also known as Mpk2), p38b and p38c, have been identified (Davis et al, 2008;Han et al, 1998a;Han et al, 1998b). As with mammalian p38s, Drosophila p38a and p38b have been shown to be activated by immune stimulation and various stressors, and flies lacking the p38a or p38b gene are susceptible to some environmental stressors (Craig et al, 2004;Cully et al, 2010;Han et al, 1998b). Recently, it has been shown that the p38a and p38b double-mutant flies are viable in nearsterile condition but hypersensitive to microbial infection (Chen et al, 2010).…”
Section: Introductionmentioning
confidence: 99%