JNK Mitogen-Activated Protein Kinases
"JNK Mitogen-Activated Protein Kinases" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.
| Descriptor ID |
D048031
|
| MeSH Number(s) |
D08.811.913.696.620.682.700.567.374 D12.644.360.450.340 D12.776.476.450.340
|
| Concept/Terms |
JNK Mitogen-Activated Protein Kinases- JNK Mitogen-Activated Protein Kinases
- JNK Mitogen Activated Protein Kinases
- jun-NH2-Terminal Kinase
- jun NH2 Terminal Kinase
- jun-NH2-Terminal Kinases
- jun NH2 Terminal Kinases
- c-jun Amino-Terminal Kinase
- Amino-Terminal Kinase, c-jun
- c jun Amino Terminal Kinase
- c-jun N-Terminal Kinase
- N-Terminal Kinase, c-jun
- c jun N Terminal Kinase
|
Below are MeSH descriptors whose meaning is more general than "JNK Mitogen-Activated Protein Kinases".
Below are MeSH descriptors whose meaning is more specific than "JNK Mitogen-Activated Protein Kinases".
This graph shows the total number of publications written about "JNK Mitogen-Activated Protein Kinases" by people in this website by year, and whether "JNK Mitogen-Activated Protein Kinases" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 1999 | 0 | 2 | 2 |
| 2005 | 0 | 1 | 1 |
| 2006 | 1 | 0 | 1 |
| 2007 | 1 | 0 | 1 |
| 2013 | 0 | 1 | 1 |
| 2016 | 1 | 0 | 1 |
| 2017 | 0 | 1 | 1 |
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Below are the most recent publications written about "JNK Mitogen-Activated Protein Kinases" by people in Profiles.
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Long-Term Alcohol-Activated c-Jun N-terminal Kinase Isoform 2 Preserves Cardiac Function but Drives Ca2+-Triggered Arrhythmias. Cells. 2023 09 08; 12(18).
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The stress kinase JNK regulates gap junction Cx43 gene expression and promotes atrial fibrillation in the aged heart. J Mol Cell Cardiol. 2018 01; 114:105-115.
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Apoptosis and Compensatory Proliferation Signaling Are Coupled by CrkI-Containing Microvesicles. Dev Cell. 2017 06 19; 41(6):674-684.e5.
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Role of galectin-1 in urinary bladder urothelial carcinoma cell invasion through the JNK pathway. Cancer Sci. 2016 Oct; 107(10):1390-1398.
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Role of mitogen-activated protein kinases and Mcl-1 in apoptosis induction by withaferin A in human breast cancer cells. Mol Carcinog. 2014 Nov; 53(11):907-16.
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c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias. Cardiovasc Res. 2013 Mar 01; 97(3):589-97.
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Impact of a high loading dose of atorvastatin on contrast-induced acute kidney injury. Circulation. 2012 Dec 18; 126(25):3008-16.
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In vivo and in vitro assessment of pathways involved in contrast media-induced renal cells apoptosis. Cell Death Dis. 2011 May 12; 2:e155.
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Guggulsterone-induced apoptosis in human prostate cancer cells is caused by reactive oxygen intermediate dependent activation of c-Jun NH2-terminal kinase. Cancer Res. 2007 Aug 01; 67(15):7439-49.
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Cis-parinaric acid effects, cytotoxicity, c-Jun N-terminal protein kinase, forkhead transcription factor and Mn-SOD differentially in malignant and normal astrocytes. Neurochem Res. 2007 Jan; 32(1):115-24.