MAPK9

(redirected from Jun kinase)

MAPK9

A gene on chromosome 5q35 that encodes a member of the MAP kinase family, which integrate multiple biochemical signals and are involved in cell proliferation, differentiation, transcription, regulation and development. MAPK9 is activated by various cell stimuli and targets specific transcription factors, mediating immediate early gene expression in response to cell stimuli. MAPK9 is closely related to MAPK8, and both are involved in UV light-induced apoptosis; MAPK9 blocks the ubiquitination of tumour suppressor p53, increasing p53 stability in non-stressed cells, and plays a key role in T cell differentiation.
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References in periodicals archive ?
Bishopric, "Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosis," Circulation Research, vol.
Bishopric, "Jun kinase delays caspase-9 activation by interaction with the apoptosome," Journal of Biological Chemistry, vol.
Webster, "Hypoxia/reoxygenation stimulates Jun kinase activity through redox signaling in cardiac myocytes," Circulation Research, vol.
Cerione, "Cdc42 and PAK-mediated signaling leads to Jun kinase and p38 mitogen-activated protein kinase activation," The Journal of Biological Chemistry, vol.
Blocking dopamine receptors controls psychotic symptoms, but neurotoxicity involves triggering apoptosis, increasing free radicals, binding to sigma receptors, increasing intracellular calcium, decreasing neurotropic factors, increasing P53, T-box, Jun kinase, etc.
11 August 2010 - Swiss specialty biopharmaceutical company PregLem said today it has signed a worldwide, exclusive in-licensing agreement for Bentamapimod, a novel, orally active, Jun Kinase Inhibitor (JNK-I AS602801) with Merck Serono,a division of Merck KGaA (ETR: MRK).
Increased Jun kinase (a protein kinase that mediates cell death)
For more than a decade, researchers have known that saturated fats activate enzymes associated with developing insulin resistance and atherosclerosis, or clogged arteries, unsaturated fats can block these enzymes within our cells and the enzymes, called Jun kinases, work at a subcellular level.
Working on this prior knowledge, a UCSD team led by Michael Karin speculated that something in cell membranes must be able to differentiate between saturated and unsaturated fats, activating or deactivating Jun kinases and in their new study, the team ultimately identified yet another enzyme, called c-Src, which resides within a cell membrane.
Three families of MAPK have been identified: the Jnk family (Jun kinases), p38 family, and Erk (extracellular signal-regulated kinase) family.
Higher doses of arsenic increase levels of jun kinases (JNKs), possibly via mitogen-activated protein kinase kinases, such as MAPKK3, and also activate MAP kinases such as extracellular signal regulated kinase (ERK3) (Cavigelli et al.