c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases
The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family and are activated by environmental stress. JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands. This pathway, therefore, can act as a critical co...
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| Format: | Online |
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Bentham Open
2012
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460413/ |
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pubmed-3460413 |
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pubmed-34604132012-10-01 c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases Guma, Monica Firestein, Gary S Article The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family and are activated by environmental stress. JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands. This pathway, therefore, can act as a critical convergence point in immune system signaling for both adaptive and innate responses. Like other MAPKs, the JNKs are activated via the sequential activation of protein kinases that includes two dual-specificity MAP kinase kinases (MKK4 and MKK7) and multiple MAP kinase kinase kinases. MAPKs, including JNKs, can be deactivated by a specialized group of phosphatases, called MAP kinase phosphatases. JNK phosphorylates and regulates the activity of transcription factors other than c-Jun, including ATF2, Elk-1, p53 and c-Myc and non-transcription factors, such as members of the Bcl-2 family. The pathway plays a critical role in cell proliferation, apoptosis, angiogenesis and migration. In this review, an overview of the functions that are related to rheumatic diseases is presented. In addition, some diseases in which JNK participates will be highlighted. Bentham Open 2012-09-07 /pmc/articles/PMC3460413/ /pubmed/23028407 http://dx.doi.org/10.2174/1874312901206010220 Text en © Guma and Firestein; Licensee Bentham Open. http://creativecommons.org/licenses/by-nc/3.0/ This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Guma, Monica Firestein, Gary S |
| spellingShingle |
Guma, Monica Firestein, Gary S c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| author_facet |
Guma, Monica Firestein, Gary S |
| author_sort |
Guma, Monica |
| title |
c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| title_short |
c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| title_full |
c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| title_fullStr |
c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| title_full_unstemmed |
c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases |
| title_sort |
c-jun n-terminal kinase in inflammation and rheumatic diseases |
| description |
The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family and are activated by environmental stress. JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands. This pathway, therefore, can act as a critical convergence point in immune system signaling for both adaptive and innate responses. Like other MAPKs, the JNKs are activated via the sequential activation of protein kinases that includes two dual-specificity MAP kinase kinases (MKK4 and MKK7) and multiple MAP kinase kinase kinases. MAPKs, including JNKs, can be deactivated by a specialized group of phosphatases, called MAP kinase phosphatases. JNK phosphorylates and regulates the activity of transcription factors other than c-Jun, including ATF2, Elk-1, p53 and c-Myc and non-transcription factors, such as members of the Bcl-2 family. The pathway plays a critical role in cell proliferation, apoptosis, angiogenesis and migration. In this review, an overview of the functions that are related to rheumatic diseases is presented. In addition, some diseases in which JNK participates will be highlighted. |
| publisher |
Bentham Open |
| publishDate |
2012 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460413/ |
| _version_ |
1611912597677801472 |