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Stress-activated Protein Kinases (stress-activated + protein_kinase)

Distribution by Scientific Domains
Medical Sciences75%

Selected Abstracts

Regulation of the immune response by stress-activated protein kinases

IMMUNOLOGICAL REVIEWS, Issue 1 2009
Mercedes Rincón
Summary:, Activation of immune cells to mediate an immune response is often triggered by potential ,danger' or ,stress' stimuli that the organism receives. Within the mitogen-activated protein kinases (MAPKs) family, the stress-activated protein kinase (SAPK) group was defined as group of kinases that activated by stimuli that cause cell stress. In the immune cells, SAPKs are activated by antigen receptors (B- or T-cell receptors), Toll-like receptors, cytokine receptors, and physical,chemical changes in the environment among other stimuli. The SAPKs are established to be important mediators of intracellular signaling during adaptive and innate immune responses. Here we summarize what is currently known about the role of two sub-groups of SAPKs , c-Jun NH2 -terminal kinase and p38 MAPK-in the function of specific components of the immune system and the overall contribution to the immune response. [source]

Neuronal p38 MAPK signalling: an emerging regulator of cell fate and function in the nervous system

GENES TO CELLS, Issue 11 2002
Kohsuke Takeda
p38 mitogen-activated protein kinases (MAPKs), together with extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs), constitute the MAPK family. Multiple intracellular signalling pathways that converge on MAPKs exist in all eukaryotic cells and play pivotal roles in a wide variety of cellular functions. p38 MAPKs and JNKs, also termed stress-activated protein kinases (SAPKs), are preferentially activated by various cytotoxic stresses and cytokines and appear to be potent regulators of stress-induced apoptosis. Whereas JNKs have been shown to play pivotal roles in the regulation of neuronal apoptosis, the role of p38 MAPKs in the nervous system is poorly understood. However, accumulating evidence from mammalian cell culture systems and the strong genetic tool C. elegans suggests that neuronal p38 signalling has diverse functions beyond the control of cell death and survival. This review focuses on possible roles for the p38 pathway in the nervous system, with principal emphasis placed on the roles in neuronal cell fate decision and function. [source]

Regulation of the immune response by stress-activated protein kinases

IMMUNOLOGICAL REVIEWS, Issue 1 2009
Mercedes Rincón
Summary:, Activation of immune cells to mediate an immune response is often triggered by potential ,danger' or ,stress' stimuli that the organism receives. Within the mitogen-activated protein kinases (MAPKs) family, the stress-activated protein kinase (SAPK) group was defined as group of kinases that activated by stimuli that cause cell stress. In the immune cells, SAPKs are activated by antigen receptors (B- or T-cell receptors), Toll-like receptors, cytokine receptors, and physical,chemical changes in the environment among other stimuli. The SAPKs are established to be important mediators of intracellular signaling during adaptive and innate immune responses. Here we summarize what is currently known about the role of two sub-groups of SAPKs , c-Jun NH2 -terminal kinase and p38 MAPK-in the function of specific components of the immune system and the overall contribution to the immune response. [source]

Low p38 MAPK and JNK activation in cultured hepatocytes of DRH rats; a strain highly resistant to hepatocarcinogenesis

MOLECULAR CARCINOGENESIS, Issue 9 2007
Satoshi Honmo
Abstract DRH rats are a hepatocarcinogenesis-resistant strain isolated from hepatocarcinogenesis-sensitive Donryu rats, and the liver of DRH shows less histological damage and fewer/smaller neoplastic hepatic lesions by the treatment with hepatocarcinogens. To investigate the mechanism of the resistance, the properties of hepatocytes of DRH and Donryu were compared. In primary culture, DRH hepatocytes exhibited higher proliferation and less apoptosis than Donryu hepatocytes in the presence of EGF and insulin. However, such difference was not correlated to the degree of DNA damage associated with cell culture or cell cycle checkpoint function. Although the mitogen-activated protein kinases [EGF receptor (EGFR) and extracellular signal regulating kinases (ERK1/2)] were activated to the same degree, the stress-activated protein kinases [p38 mitogen-activated protein kinase (p38) and c- jun N-terminal kinase (JNK)] were activated to a lesser degree in the DRH hepatocytes. Treatment with 2-acetylaminofluorene (2-AAF) in vivo also resulted in less JNK and p38 activation in the DRH livers. Furthermore, apoptosis signal-regulating kinase 1 (ASK1) was inhibited by the lysate from the DRH but not by the Donryu hepatocytes. The low activation of the stress-activated protein kinases may be linked to the resistance to cellular stress, which may underlie the hepatocarcinogenesis-resistance in DRH rats. © 2007 Wiley-Liss, Inc. [source]