The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
p38 MAP-Kinases pathway regulation, function and role in human diseases
Open accessAbstract
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.
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Independent Human MAP-Kinase Signal Transduction Pathways Defined by MEK and MKK Isoforms
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Reactive oxygen species act through p38 MAPK to limit the lifespan of hematopoietic stem cells
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“JIP2 can bind to JNK and to the other components of this pathway, MKK7 and MLK3 [63], but also binds to MKK3, p38α and p38δ MAPKs [64–66].”
BackgroundSignalling specificity of Ser/Thr protein kinases through docking-site-mediated interactions
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Alternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinases
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Self-citation
Cited by
Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases
Cargnello, M., & Roux, P. P. (2011) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00031-10 · Cited by 3,274
Inflammatory networks during cellular senescence: causes and consequences.
Freund, A., Orjalo, A. V., Desprez, P.-Y., & Campisi, J. (2010) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2010.03.003 · Cited by 1,354
Understanding MAPK Signaling Pathways in Apoptosis
Yue, J., & López, J. M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21072346 · Cited by 1,245
Freund, A., Patil, C. K., & Campisi, J. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.69 · Cited by 1,039
Glucocorticoid resistance in inflammatory diseases
Barnes, P. J., & Adcock, I. M. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60326-3 · Cited by 983
Metadata
- Authors
- Cuenda, A., & Rousseau, S.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2007-08
- Volume
- 1773
- Issue
- 8
- Pages
- 1358-1375
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W1965909642
- Cited by
- 1,400
- References
- 10
- FWCI
- 22.03
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
