JNK and Human Diseases . Its activation contributes to inflammation, apoptosis, cell differentiation, and cell cycle regulation. There are three different JNK isoforms (JNK-1, -2, and -3), which belong to MAPK family. Remarkably, many of these conditions have mirrored the data from the JNK knockout animals, indicating the high level of consistency between the human and mouse systems.
identified p38 MAPK as the de-repressive link between inflammation and autophagy 4.
Activated JNK and p38 translocate to the nucleus where they activate multiple transcription factors, via MSK1/2 in the case of p38, including AP-1, ATF2, CREB, ATF1, and NF-kappa B. The activation of these transcription factors results in the transcription of genes encoding proinflammatory cytokines. Recently, He et. JNK. al.
Like JNK pathway, p38 signaling are strongly activated by environmental stresses and inflammatory cytokines. The disease groups can be divided into the following main areas: neurological, coronary, hepatobiliary, and respiratory diseases; and autoimmune, inflammatory, and cancer conditions.
Eur Rev Med Pharmacol Sci 2019; 23 (17): 7655-7662 DOI: 10.26355/eurrev_201909_18889 TLR4 promotes liver inflammation by activating the JNK pathway To evaluate the role of MAPK/JNK pathway in TMAO-induced formation of foam cells, PEMs were pretreated with p38 MAPK inhibitor (SB203580) or JNK inhibitor (SP600125) for 1 h, then were incubated with ox-LDL (50 μg/ml) and TMAO (100 μmol/L) for 24 h. RAW264.7 was purchased from ATCC (USA). JNK Pathway. Dysregulation of JNK pathway is associated with a wide range of immune disorders and cancer. The p38 family members possess a TGY motif in the activation segment. However, the function of JNKs in bacteria-induced intestinal inflammation is still poorly understood.
The c-Jun NH2-terminal kinases (JNKs) are an evolutionarily conserved family of serine/threonine protein kinases that play critical roles in the pathological process in species ranging from insects to mammals. Objective: This study aimed to investigate the correlation of serum Jun-amino-terminal kinase (JNK) pathway-associated phosphatase (JKAP) level with disease risk, severity, inflammation, and treatment response to tumor necrosis factor (TNF)-α inhibitor in Crohn disease (CD) patients.. The c-Jun N-terminal kinases (JNKs), with its members JNK1, JNK2, and JNK3, is a subfamily of (MAPK) mitogen-activated protein kinases. JNK signaling regulates a wide range of cellular processes, including cell proliferation, differentiation, survival, apoptosis, and inflammation.
Pathway Description: Stress-activated protein kinases (SAPK)/Jun amino-terminal kinases (JNK) are members of the MAPK family and are activated by a variety of environmental stresses, inflam- matory cytokines, growth factors, and GPCR agonists.
3.2. However, it remains unclear how inflammation can evade the negative regulation of autophagy and under what conditions this might occur.
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