Biological Information
Background Information:
c-Jun N-terminal kinases (JNKs), a stress-activated protein kinase (SAPK), is involved in cellular responses to environmental stresses. JNK kinases can be activated by stimuli such as UV light, radiation, protein synthesis inhibitors, ceramide, DNA-damaging drugs, chemopreventive drugs, TNF-a, and interleukin 1. JNK binds to an NH2-terminal region of ATF2 and c-Jun and phosphorylates two sites within the activation domain of each transcription factor. Three JNK genes (Jnk1, -2 and -3) have been identified in humans; however, splice variants result in a total of 10 isoforms. Therapeutic inhibition of JNK may provide clinical benefit in diseases as diverse as immune inflammatory (joint, bowel, pulmonary), ischemic injury (brain, cardiac) and neurodegenerative (Alzheimer's, Parkinson's) diseases. EMBL L31951. Recombinant protein contains the amino acid residue substitution S51N with respect to EMBL L31951. This conflict is reported in GenBank U09759 and the following GenBank ESTs, AL532378, AL550761, BI333490.
Target Class:
Kinase
Family:
CMGC
Sub Family:
Protein Ser/Thr
Protein Name:
JNK2
Protein Aliases:
Jun kinase
Accession Number:
NM_002752.3; NM_139068.1; NM_139069.1; NM_139070.1
UniProt Number:
P45984
Gene Name:
MAPK9
Gene ID:
5601
Gene Aliases:
JNK2|p54a|SAPK|PRKM9|SAPK1A
Target Species:
Human
Usage
Product Type:
Enzymes
Application:
Drug Discovery & Development
Storage Conditions:
6 months at -70°C
Usage disclaimer:
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Assay Information
Assay Type:
Enzymatic
Clinical Relevance
Therapeutic Area:
Oncology/Immuno-Oncology