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