Activation of SAPK/JNKs in vitro.
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Summary
The stress-activated protein kinase/c-jun N-terminal kinases (SAPK/JNKs) are mitogen-activatedprotein kinases that are activated by stressful and inflammatory stimuli and regulate cellular responses such as proliferation, differentiation, and apoptosis.
- Type
- article
- Published
- 2010-01-01
- Cited by
- 12
- References
- 23
- OpenAlex
- https://openalex.org/W138881307
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:22700877
Keywords
Cell biology, Kinase, p38 mitogen-activated protein kinases, MAP kinase kinase kinase, Mitogen-activated protein kinase
References
- Scaffold proteins in mammalian MAP kinase cascades.
- The stress-activated protein kinases are major c-Jun amino-terminal kinases activated by ischemia and reperfusion.
- JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain.
- Evidence for a Role of Rho-like GTPases and Stress-activated Protein Kinase/c-Jun N-terminal Kinase (SAPK/JNK) in Transforming Growth Factor β-mediated Signaling*
- Secondary and Tertiary Structure Changes of Reconstituted P-glycoprotein
- Activation of p38 Mitogen-activated Protein Kinase by c-Abl-dependent and -independent Mechanisms*
- Induction of Apoptosis by DPC4, a Transcriptional Factor Regulated by Transforming Growth Factor-β through Stress-activated Protein Kinase/c-Jun N-terminal Kinase (SAPK/JNK) Signaling Pathway*
- The stress-activated protein kinase subfamily of c-Jun kinases
- An osmosensing signal transduction pathway in mammalian cells.
- GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38
- Gene 33/Mig-6, a Transcriptionally Inducible Adapter Protein That Binds GTP-Cdc42 and Activates SAPK/JNK*
- Sounding the Alarm: Protein Kinase Cascades Activated by Stress and Inflammation*
- The Seven-transmembrane-spanning Receptors for Endothelin and Thrombin Cause Proliferation of Airway Smooth Muscle Cells and Activation of the Extracellular Regulated Kinase and c-Jun NH-terminal Kinase Groups of Mitogen-activated Protein Kinases (*)
- Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.
- JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis
- MLK3 is required for mitogen activation of B-Raf, ERK and cell proliferation
- Dissection of a Signaling Pathway by Which Pathogen-associated Molecular Patterns Recruit the JNK and p38 MAPKs and Trigger Cytokine Release*
- Germinal Center Kinase Is Required for Optimal Jun N-Terminal Kinase Activation by Toll-Like Receptor Agonists and Is Regulated by the Ubiquitin Proteasome System and Agonist-Induced, TRAF6-Dependent Stabilization
- Regulation of MAP kinase signaling modules by scaffold proteins in mammals.
- Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation.
Cited by
- miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4–JNK pathway
- The protective effect of 17β-estradiol against hydrogen peroxide-induced apoptosis on mesenchymal stem cell.
- Building on the foundation of daring hypotheses: Using the MKK4 metastasis suppressor to develop models of dormancy and metastatic colonization
- DGCR8 mediates repair of UV-induced DNA damage independently of RNA processing
- PlMAPK10, a Mitogen-Activated Protein Kinase (MAPK) in Peronophythora litchii, Is Required for Mycelial Growth, Sporulation, Laccase Activity, and Plant Infection
- The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer
- Human Papillomavirus and Cellular Pathways: Hits and Targets
- The Hallmarks of Flavonoids in Cancer
- The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases
- Circ_0084043-miR-134-5p axis regulates PCDH9 to suppress melanoma
- Regulation of the microglial polarization for alleviating neuroinflammation in the pathogenesis and therapeutics of major depressive disorder.
- PALACKY UNIVERSITY OLOMOUC Faculty of Natural Sciences Department of Biochemistry The effect of graphene oxide on the pregnane X receptor signaling pathway regulating the biotransformation of xenobiotics
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