JNK Mitogen-Activated Protein Kinases

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.

Also Known As:

c-jun Amino-Terminal Kinase; c-jun N-Terminal Kinase; jun-NH2-Terminal Kinase; jun-NH2-Terminal Kinases; Amino-Terminal Kinase, c-jun; JNK Mitogen Activated Protein Kinases; Kinase, jun N-Terminal; N-Terminal Kinase, c-jun; N-Terminal Kinase, jun; c jun Amino Terminal Kinase; c jun N Terminal Kinase; jun N Terminal Kinase; jun NH2 Terminal Kinase; jun NH2 Terminal Kinases; jun N-Terminal Kinase

Networked: 2029 relevant articles (40 outcomes, 183 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Bonny, Christophe: 14 articles (05/2012 - 09/2003)
2.	Zhang, Wei: 10 articles (01/2022 - 09/2011)
3.	Zhang, Guang-Yi: 10 articles (04/2012 - 02/2005)
4.	Bennett, Brydon L: 9 articles (12/2021 - 12/2003)
5.	Zhang, Yi: 9 articles (01/2021 - 02/2008)
6.	Borsello, Tiziana: 9 articles (11/2018 - 09/2003)
7.	Kim, Myeong Ok: 8 articles (06/2021 - 03/2016)
8.	Nikolic-Paterson, David J: 8 articles (01/2021 - 02/2007)
9.	Davis, Roger J: 7 articles (01/2022 - 12/2003)
10.	Li, Ning: 7 articles (01/2022 - 10/2002)

Related Diseases

1.	Insulin Resistance 05/01/2021 - "We found that Wnt/c-Jun N-terminal kinase signaling was closely associated with insulin resistance, inflammatory response, and pancreatic β-cell and endothelial dysfunction. " 01/01/2020 - "hypertrophy), mitochondrial H2 O2 emission, oxidative stress, c-Jun N-terminal kinase phosphorylation and leucocyte infiltration, and induced insulin resistance. " 01/01/2018 - "Treatment of differentiated C2C12 cells with recombinant HPS caused c-Jun N-terminal kinase (JNK) phosphorylation and impairment of insulin sensitivity in a dose-dependent manner. " 06/01/2017 - "The 1PL and 4PL groups showed increase in macrophage content, IKKα/β, and Jun N-terminal kinase phosphorylation status, serum LPS and HSP70 levels, and insulin resistance and no changes in glycemia and insulinemia compared with the control group. " 10/01/2016 - "Furthermore, c-Jun N-terminal kinase activation, which plays a pivotal role in insulin resistance and AD pathologies, is significantly inhibited. "
2.	Inflammation (Inflammations) 01/01/2023 - "Furthermore, our study demonstrated that SIL ameliorates intestinal inflammation via modulating the c-Jun N-terminal kinase (JNK) signaling pathway in Drosophila. " 11/20/2023 - "To sum up, Dex improved POCD by considering CEBPB as a drug target to activate the c-Jun N-terminal kinase (JNK)/p-38 signaling pathway, inhibiting microglial M1 polarization-mediated inflammation in the central nervous system." 01/01/2020 - "Fish c-Jun N-Terminal Kinase (JNK) Pathway Is Involved in Bacterial MDP-Induced Intestinal Inflammation." 01/01/2018 - "It may involve microglia deactivation and inflammation inhibition in the spinal cord, in which the proliferator-activated receptor gamma/p38/Jun N-terminal kinase pathway is activated. " 01/01/2018 - "The mechanism of H2S preconditioning may involve microglia deactivation and inflammation inhibition in the spinal cord, in which the proliferator-activated receptor gamma/p38/Jun N-terminal kinase pathway is activated. "
3.	Brain Injuries (Brain Injury) 10/01/2016 - "Therefore, the aim of this study was to investigate the neuroprotective mechanisms of BP against ischemic brain injury induced by cerebral I/R through inhibition of the c-Jun N-terminal kinase (JNK)-Caspase3 signaling pathway. " 12/01/2013 - "Previous studies have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. " 05/12/2006 - "Our previous studies and the others have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. " 01/30/2006 - "Our previous studies and those of others have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. " 01/01/2018 - "It is well known that Wnt5a activation plays a pivotal role in brain injury and β-arrestin2 induces c-Jun N-terminal kinase (JNK3) activation is involved in neuronal cell death. "
4.	Brain Ischemia (Cerebral Ischemia) 05/03/2019 - "Protective Effects of a New C-Jun N-terminal Kinase Inhibitor in the Model of Global Cerebral Ischemia in Rats." 11/01/2013 - "The c-Jun N-terminal kinase (JNK) undergoes complete inactivation following the intense activation induced by cerebral ischemia and reperfusion in rat hippocampi. " 06/13/2012 - "Delayed inhibition of c-Jun N-terminal kinase worsens outcomes after focal cerebral ischemia." 01/06/2012 - "In this work, we investigated whether HO-1 was involved in the regulation of the c-Jun N-terminal kinase (JNK) signaling pathway and neuronal cell injury induced by the brain ischemia followed by reperfusion. " 10/01/2011 - "C-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in cerebral ischemia. "
5.	Necrosis 04/01/2009 - "In the present study, we show that IL-1beta-induced apoptosis and necrosis in primary rat beta-cells and MIN6 cells largely depends on ER stress, ER Ca(2+) release, and c-Jun N-terminal kinase (JNK) activation. " 01/01/2019 - "The Role of Phospho-c-Jun N-Terminal Kinase Expression on hepatocyte Necrosis and Autophagy in the Cholestatic Liver." 01/01/2018 - "Lipotoxicity kills hepatocytes by apoptosis, a highly regulated, non-inflammatory form of cell death, but also by necrosis, necroptosis and pyroptosis; the latter involve mitochondrial injury, oxidative stress, activation of c-Jun N-terminal kinase (JNK) and release of danger-associated molecular patterns (DAMPs). " 01/01/2012 - "The inhibition of c-Jun N-terminal Kinase and p38 attenuated CD154-mediated apoptosis but not necrosis. " 12/07/2009 - "We also showed that the expression of active mutant IPP5 in HeLa cells was further enhanced on TNF (tumour necrosis factor) treatment and overexpression of active mutant IPP5 sensitized HeLa cells to TNF-induced JNK (c-Jun N-terminal kinase) and p38 activation as well as TNF-mediated apoptosis. "

Related Drugs and Biologics

1.	Phosphotransferases (Kinase)
2.	Extracellular Signal-Regulated MAP Kinases (Extracellular Signal Regulated Kinases)
3.	Proteins (Proteins, Gene)
4.	NF-kappa B (NF-kB)
5.	Reactive Oxygen Species (Oxygen Radicals)
6.	Insulin (Novolin)
7.	p38 Mitogen-Activated Protein Kinases
8.	Glucose (Dextrose)
9.	Interleukin-1beta (Interleukin 1 beta)
10.	Mitogen-Activated Protein Kinases

Related Therapies and Procedures

1.	Therapeutics
2.	Drug Therapy (Chemotherapy)
3.	Ligation
4.	Intraperitoneal Injections
5.	Negative-Pressure Wound Therapy