The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Non-Classical P38 Map Kinase Functions: Cell Cycle Checkpoints and Survival
Open accessAbstract
The p38 MAPK kinase pathway is activated in response to a wide range of cellular stress stimuli and cytokines. Our understanding of the important functions of p38 MAPK in the process of differentiation and cell death has grown considerably in the recent years and is now relatively established. Here we discuss the role of p38 MAPK in the mediation of cell cycle checkpoints and cell survival, processes that have received less attention. We describe how p38 MAPK regulates both the G2/M as well as a G1/S cell cycle checkpoint in response to cellular stress such as DNA damage. While p38 MAPK has classically been associated with the induction of apoptosis, we discuss that p38 MAPK can also mediate cell survival in specific situations, such as in response to DNA damage. It is important to recognize these less appreciated functions of p38 MAPK when considering the potential use of pharmacological inhibitors of p38 MAPK in therapeutic treatments for disease.
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Cites
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The DNA damage response: putting checkpoints in perspective
Zhou, B.-B. S., & Elledge, S. J. (2000) · Nature · doi:10.1038/35044005 · Cited by 3,213
Differential regulation and properties of MAPKs
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“The family of mitogen activated protein kinases (MAPKs) is composed of three major groups: the extracellular regulated kinases (ERKs), the C-Jun N-terminal Kinases (JNKs) and the p38 MAPKs [1].”
BackgroundReactive oxygen species act through p38 MAPK to limit the lifespan of hematopoietic stem cells
Ito, K., Hirao, A., Arai, F., Takubo, K., Matsuoka, S., Miyamoto, K., Ohmura, M., Naka, K., Hosokawa, K., Ikeda, Y., et al. (2006) · Nature Medicine · doi:10.1038/nm1388 · Cited by 1,362
The JNK signal transduction pathway
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Phosphorylation by p38 MAPK as an Alternative Pathway for GSK3β Inactivation
Thornton, T. M., Pedraza-Alva, G., Deng, B., Wood, C. D., Aronshtam, A., Clements, J. L., Sabio, G., Davis, R. J., Matthews, D. E., Doble, B., et al. (2008) · Science · doi:10.1126/science.1156037 · Cited by 484
Self-citationAlternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinases
Salvador, J. M., Mittelstadt, P. R., Guszczynski, T., Copeland, T. D., Yamaguchi, H., Appella, E., Fornace, A. J., & Ashwell, J. D. (2005) · Nature Immunology · doi:10.1038/ni1177 · Cited by 306
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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
Keshet, Y., & Seger, R. (2010) · Methods in Molecular Biology · doi:10.1007/978-1-60761-795-2_1 · Cited by 642
Tau protein kinases: Involvement in Alzheimer's disease
Martin, L., Latypova, X., Wilson, C. M., Magnaudeix, A., Perrin, M.-L., Yardin, C., & Terro, F. (2013) · Ageing Research Reviews · doi:10.1016/j.arr.2012.06.003 · Cited by 631
The Two Faces of Reactive Oxygen Species in Cancer
Reczek, C. R., & Chandel, N. S. (2017) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-041916-065808 · Cited by 602
“ROS-mediated activation of the JNK and p38 signaling pathways can also induce cell cycle arrest, preventing cancer cell growth and division (Ambrosino & Nebreda 2001, Thornton & Rincon 2009, Wagner & Nebreda 2009).”
BackgroundROS in Cancer: The Burning Question
Chio, I. I. C., & Tuveson, D. A. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.03.004 · Cited by 532
Metadata
- Authors
- Thornton, T. M., & Rincon, M.
- Venue
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Published
- 2009
- Volume
- 5
- Issue
- 1
- Pages
- 44-52
- ISSN
- 1449-2288 (ISSN-L)
- OpenAlex
- W2152476041
- Cited by
- 443
- References
- 8
- FWCI
- 14.88
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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