By Product Type
By Research Area
All the posters in the Proteintech library are available in PDF format or can be requested as a hard copy.
JNKs (c-Jun N-terminal kinases), also known as stress-activated protein kinases, are a subfamily of mitogen-activated protein (MAP) kinases. They are strongly stimulated by numerous environmental stresses but also by mitogens, inflammatory cytokines, oncogenes, and inducers of cell differentiation or morphogenesis (1).
Three major genes have been identified as regulators of the JNK pathway. JNK1 and JNK2 have broad tissue distribution and play a significant role in insulin resistance, inflammation, and cell signaling. JNK3 is predominantly found in the central nervous system (CNS) neurons. The JNKs are activated by phosphorylation on threonine and tyrosine residues via MKK4 and MKK7; inactivation of the JNKs is induced by MAPK phosphatases, which usually function in a negative feedback loop (2).
Since deregulation of JNK is linked with various diseases, including neurodegenerative disorders (Parkinson’s, Alzheimer’s), diabetes, cancer, cardiac hypertrophy, and asthma, JNK inhibitors, activators, and isoforms have a potential as therapeutic targets. (3)