In certain cases of stress, the MAPK, p38 MAPK, and JNK cascades may be activated. These cascades originate from a stress signal, such as nitric oxide, reactive oxygen species, calcium overload, and ER stress, causing ligand binding to a receptor tyrosine kinase, which leads to dimerization and the self-phosphorylation of the kinases. GRB2 and SOS bind to the kinase complex, which leads to the activation of Ras as GDP is phosphorylated to GTP. This can lead to the activation of multiple cascades, and in the case of the p38 pathway, various forms of MMK are activated, which in turn activated p38 isoforms and induce several activities inside the nucleus. Some of these activities include stress responses such as cell death, differentiation, and increase in cytokine production, and several stress-related MAPK pathways can help in instances of high osmolarity, heat, and oxidative stress.
Stress-activated Mapk Cascade Bioinformatics Tool
Laverne is a handy bioinformatics tool to help facilitate scientific exploration of related genes, diseases and pathways based on co-citations. Explore more on Stress-activated Mapk Cascade below!
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We have 295 products for the study of the Stress-activated Mapk Cascade Pathway that can be applied to Chromatin Immunoprecipitation, Flow Cytometry, Western Blot, Immunocytochemistry/Immunofluorescence, Immunohistochemistry from our catalog of antibodies and ELISA kits.