Results 261 to 270 of about 195,376 (282)

c-Jun N-terminal kinase regulates CTP:phosphocholine cytidylyltransferase

Archives of Biochemistry and Biophysics, 2006
CTP:phosphocholine cytidylyltransferase (CCTalpha) is a rate-regulatory enzyme required for phosphatidylcholine (PtdCho) synthesis. CCTalpha is also a phosphoenzyme, but the physiologic role of kinases on enzyme function remains unclear. We report high-level expression of two major isoforms of the c-Jun N-terminal kinase family (JNK1 and JNK2) in ...
Alan J, Ryan, Matthew, Andrews, Jiming, Zhou, Rama K, Mallampalli   +3 more
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Nitric Oxide Modulates the c-Jun N-terminal Kinase/Stress-Activated Protein Kinase Activity through Activating c-Jun N-Terminal Kinase Kinase

Biochemistry, 1997
Nitric oxide is a signaling molecule that has a broad range of physiological functions, including neurotransmission, macrophage activation, and vasodilation. The mechanism by which nitric oxide regulates signal transduction mediating diverse biological activities is not fully understood, however.
H, Kim, J, Shim, P L, Han, E J, Choi
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Recent Advances in c-Jun N-Terminal Kinase (JNK) Inhibitors

Current Medicinal Chemistry, 2021
c-Jun N-Terminal Kinases (JNKs), members of the Mitogen-Activated Protein Kinase (MAPK) signaling pathway, play a key role in the pathogenesis of many diseases including cancer, inflammation, Parkinson’s disease, Alzheimer’s disease, cardiovascular disease, obesity, and diabetes.
Gang Li, Wenqing Qi, Xiaoxun Li, Jinwu Zhao, Meihua Luo, Jianjun Chen   +5 more
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Mechanistic characterization for c-jun-N-Terminal Kinase 1α1

Archives of Biochemistry and Biophysics, 2008
c-jun-N-terminal kinase 1alpha1 (JNK1alpha1) is a serine/threonine kinase of the mitogen-activated protein (MAP) kinase family that phosphorylates protein transcription factors after activation by a variety of environmental stressors. In this study, the kinetic mechanism for JNK1alpha1 phosphorylation of activating transcription factor 2 (ATF2) was ...
Brian, Ember, Philip, LoGrasso
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Inhibitors of c-Jun N-Terminal Kinases: An Update

Journal of Medicinal Chemistry, 2014
The c-Jun N-terminal kinases (JNKs) are serine/threonine kinases implicated in the pathogenesis of various diseases. Recent advances in the development of novel inhibitors of JNKs will be reviewed. Significant progress in the design of JNK inhibitors displaying selectivity versus other kinases has been achieved within the past 4 years.
Koch, Pierre, Gehringer, Matthias, Laufer, Stefan   +2 more
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c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis

Canadian Journal of Physiology and Pharmacology, 2014
Osteoarthritis (OA) is a chronic degenerative joint disorder. Previous studies have shown abnormally increased apoptosis of chondrocytes in patients and animal models of OA. TNF-α and nitric oxide have been reported to induce chondrocyte ageing; however, the mechanism of chondrocyte apoptosis induced by IL-1β has remained unclear.
Zhiqiang, Ye, Yuxian, Chen, Rongkai, Zhang, Haitao, Dai, Chun, Zeng, Hua, Zeng, Hui, Feng, Gengheng, Du, Hang, Fang, Daozhang, Cai   +9 more
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c-Jun N-terminal kinases in memory and synaptic plasticity

revneuro, 2011
Abstract The c-Jun N-terminal kinases (JNK) belong to the subfamily of mitogen-activated protein kinases (MAPK). JNK is an important signaling enzyme that is involved in many facets of cellular regulation including gene expression, cell proliferation and programmed cell death.
Sherrin, Tessi, Blank, Thomas, Todorovic, Cedomir   +2 more
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c-Jun N-Terminal Kinase Pathway Inhibition in Intracerebral Hemorrhage

Cerebrovascular Diseases, 2010
<i>Background:</i> Inhibition of the c-Jun N-terminal kinase (JNK) pathway by the TAT-coupled peptide XG-102 (formerly D- JNKI1) induces strong neuroprotection in ischemic stroke in rodents. We investigated the effect of JNK inhibition in intracerebral hemorrhage (ICH).
Delphine, Michel-Monigadon, Christophe, Bonny, Lorenz, Hirt   +2 more
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Arrestin‐3‐Dependent Activation of c‐Jun N‐Terminal Kinases (JNKs)

Current Protocols, 2023
AbstractOnly 1 out of 4 mammalian arrestin subtypes, arrestin‐3, facilitates the activation of c‐Jun N‐terminal kinase (JNK) family kinases. Here, we describe two different sets of protocols used for elucidating the mechanisms involved. One is based on reconstitution of signaling modules from the following purified proteins: arrestin‐3, MKK4, MKK7 ...
Xuanzhi, Zhan, Tamer S, Kaoud, Kevin N, Dalby, Eugenia V, Gurevich, Vsevolod V, Gurevich   +4 more
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c-Jun N-terminal kinases as potential therapeutic targets

Expert Opinion on Therapeutic Targets, 2007
One principal aim of research in the signal transduction field is to identify targets for therapeutic intervention, in an attempt to modify disease and curtail human suffering. Diseases such as chronic inflammation, atherosclerosis, diabetes and cancer exact a huge toll on health, in physical, social and financial terms.
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