Enzymes
Product List
JNK2/SAPK1 Human
JNK2/SAPK1 Human Recombinant
SAPK1/JNK2 is purified by proprietary chromatographic techniques.
Introduction
Jun N-terminal Kinase (JNK), also known as Stress-Activated Protein Kinase (SAPK), is a member of the Mitogen-Activated Protein Kinase (MAPK) family. JNKs are responsive to stress stimuli such as cytokines, ultraviolet irradiation, heat shock, and osmotic shock. They were originally identified as kinases that bind and phosphorylate the c-Jun protein on serine residues within its transcriptional activation domain . JNKs are classified into three main isoforms: JNK1, JNK2, and JNK3, each encoded by separate genes (MAPK8, MAPK9, and MAPK10 respectively) .
JNKs exhibit distinct expression patterns and tissue distribution. JNK1 and JNK2 are ubiquitously expressed in all cells and tissues, while JNK3 is predominantly found in the brain, heart, and testes . The activation of JNKs involves dual phosphorylation on threonine and tyrosine residues, which is mediated by upstream kinases MKK4 and MKK7 . JNKs play a crucial role in cellular responses to stress, including apoptosis, differentiation, and proliferation .
JNKs regulate a variety of biological processes. They are involved in cell proliferation, apoptosis, autophagy, and inflammation . JNKs play a significant role in immune responses by modulating the activity of transcription factors such as c-Jun, which in turn regulates the expression of genes involved in immune and inflammatory responses . Additionally, JNKs are implicated in pathogen recognition and the cellular response to infections .
JNKs interact with various molecules and cells through complex signaling pathways. Upon activation, JNKs translocate to the nucleus where they phosphorylate transcription factors such as c-Jun, ATF2, and Elk1 . This phosphorylation leads to the activation of downstream signaling cascades that regulate gene expression . JNKs also interact with scaffold proteins like JNK-interacting proteins (JIPs), which facilitate the assembly of signaling complexes and enhance the specificity of JNK signaling .
The expression and activity of JNKs are tightly regulated by multiple mechanisms. Transcriptional regulation involves the activation of upstream kinases and the binding of transcription factors to the promoter regions of JNK genes . Post-translational modifications, such as phosphorylation, ubiquitination, and acetylation, also play a critical role in modulating JNK activity . Additionally, feedback mechanisms involving phosphatases and other regulatory proteins ensure the precise control of JNK signaling .
JNKs have significant applications in biomedical research, diagnostics, and therapeutics. In research, JNKs are studied for their roles in various diseases, including cancer, neurodegenerative disorders, and inflammatory diseases . Diagnostic tools targeting JNK pathways are being developed to detect and monitor disease progression . Therapeutically, JNK inhibitors are being explored as potential treatments for conditions such as Alzheimer’s disease, diabetes, and cancer .
JNKs play a vital role throughout the life cycle, from development to aging and disease. During development, JNKs are involved in processes such as cell differentiation and organogenesis . In adulthood, JNKs contribute to the maintenance of cellular homeostasis and the response to environmental stress . As organisms age, dysregulation of JNK signaling has been linked to age-related diseases, including neurodegenerative disorders and cancer .
