The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Regulation of the immune response by stress‐activated protein kinases
Abstract
Summary: Activation of immune cells to mediate an immune response is often triggered by potential ‘danger’ or ‘stress’ stimuli that the organism receives. Within the mitogen‐activated protein kinases (MAPKs) family, the stress‐activated protein kinase (SAPK) group was defined as group of kinases that activated by stimuli that cause cell stress. In the immune cells, SAPKs are activated by antigen receptors (B‐ or T‐cell receptors), Toll‐like receptors, cytokine receptors, and physical–chemical changes in the environment among other stimuli. The SAPKs are established to be important mediators of intracellular signaling during adaptive and innate immune responses. Here we summarize what is currently known about the role of two sub‐groups of SAPKs – c‐Jun NH 2‐terminal kinase and p38 MAPK‐in the function of specific components of the immune system and the overall contribution to the immune response.
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Cites
Regulation of Phagosome Maturation by Signals from Toll-Like Receptors
Blander, J. M., & Medzhitov, R. (2004) · Science · doi:10.1126/science.1096158 · Cited by 991
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-citationMAP kinase phosphatase 1 controls innate immune responses and suppresses endotoxic shock
Zhao, Q., Wang, X., Nelin, L. D., Yao, Y., Matta, R., Manson, M. E., Baliga, R. S., Meng, X., Smith, C. V., Bauer, J. A., et al. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20051794 · Cited by 370
Nuclear Accumulation of NFAT4 Opposed by the JNK Signal Transduction Pathway
Chow, C.-W., Rincón, M., Cavanagh, J., Dickens, M., & Davis, R. J. (1997) · Science · doi:10.1126/science.278.5343.1638 · Cited by 357
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
The JNK Are Important for Development and Survival of Macrophages
Himes, S. R., Sester, D. P., Ravasi, T., Cronau, S. L., Sasmono, T., & Hume, D. A. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.176.4.2219 · Cited by 117 · cited 1×
“Although pharmacological inhibitors and peptide inhibitors of JNK have been shown to induce apoptosis of macrophages and inhibit colony-stimulating factor (CSF-1)dependent differentiation of bone marrow cells into macrophages (37), no defect in macrophage differentiation has been reported in JNK-deficient mice.”
Backgroundc-Jun N-terminal kinase-dependent mechanisms in respiratory disease
Bennett, B. L. (2006) · European Respiratory Journal · doi:10.1183/09031936.06.00012106 · Cited by 63
Cited by
Diversity and versatility of p38 kinase signalling in health and disease
Canovas, B., & Nebreda, A. R. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00322-w · Cited by 657
Dual‐specificity MAP kinase phosphatases (MKPs): Shaping the outcome of MAP kinase signalling
Caunt, C. J., & Keyse, S. M. (2013) · The FEBS Journal · doi:10.1111/j.1742-4658.2012.08716.x · Cited by 535
MAPK signaling in inflammation-associated cancer development
Huang, P., Han, J., & Hui, L. (2010) · Protein & Cell · doi:10.1007/s13238-010-0019-9 · Cited by 273
Kietzmann, T., Mennerich, D., & Dimova, E. Y. (2016) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2016.00011 · Cited by 176
JNK signaling is converted from anti- to pro-tumor pathway by Ras-mediated switch of Warts activity
Enomoto, M., Kizawa, D., Ohsawa, S., & Igaki, T. (2015) · Developmental Biology · doi:10.1016/j.ydbio.2015.05.001 · Cited by 74
Metadata
- Authors
- Rincón, M., & Davis, R. J.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2009-03
- Volume
- 228
- Issue
- 1
- Pages
- 212-224
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W1980926721
- Cited by
- 266
- References
- 7
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- closed
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