p38 MAP-kinases pathway regulation, function and role in human diseases.
By A. Cuenda, S. Rousseau. Biochimica et Biophysica Acta, 2007
1,411 citations recorded by the source corpus.
Mammalian p38 mitogen-activated protein kinases (MAPKs) are activated by a wide range of cellular stresses as well as in response to inflammatory cytokines. There are four members of the p38MAPK family (p38alpha, p38beta, p38gamma and p38delta) which are about 60% identical in their amino acid sequence but differ in their expression patterns, substrate specificities and sensitivities to chemical inhibitors such as SB203580. A large body of evidences indicates that p38MAPK activity is critical for normal immune and inflammatory response. The p38MAPK pathway is a key regulator of pro-inflammatory cytokines biosynthesis at the transcriptional and translational levels, which makes different components of this pathway potential targets for the treatment of autoimmune and inflammatory diseases. However, recent studies have shed light on the broad effect of p38MAPK activation in the control of many other aspects of the physiology of the cell, such as control of cell cycle or cytoskeleton remodelling. Here we focus on these emergent roles of p38MAPKs and their implication in different pathologies.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7135e81eba5b2efb9ef561662097b35211b4a788
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Citations in the corpus
- The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, background): “Indeed, p38s were found to act as a key component in the induction of in fl ammation, and are currently considered as important therapeutic targets for in fl am-mation-related diseases [60,61].”
- Signal integration by JNK and p38 MAPK pathways in cancer development (2009, background): “Most of the published literature on p38 MAPKs refers to p38&alpha”
- p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “lation in response to a variety of stresses (Cuenda and Rousseau, 2007), including oncogenic RAS (Ha-RAS)”
- MAP kinase pathways. (2012, background): “p38 activation contributes to inflammation, apoptosis, cell differentiation, and cell cycle regulation (Cuenda and Rousseau 2007; Cuadrado and Nebreda 2010).”
- Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “p38MAPK is a member of the mitogen-activated protein kinase (MAPK) family, which responds to a wide variety of extracellular and intracellular signals [59].”
- TNF and MAP kinase signaling pathways (2014, neutral): “These p38 MAPKs are strongly activated by exposure to stress and by inflammatory cytokines, including TNFα [93].”
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions (2022, background): “MAPK is another important regulator of autophagy associated with ischemic stroke.(161) MAPKs act as upstream regulators of mTORC1 and modulate autophagy through the MAPK/mTOR signaling pathway in ischemic stroke.”
- Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases (2011, background): “These effects can be mediated by transcriptional and posttranscriptional mechanisms, which affect death receptors, survival pathways or pro- and antiapoptotic Bcl-2 family proteins (77).”
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “Physiologically, this translates into a role for p38 in chronic inflammatory diseases (rheumatoid arthritis, Crohn’s disease, psoriasis, and chronic asthma), tumorgenesis, cardiovascular disease, and Alzheimer’s disease (83).”