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MAP2K7 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signalling pathway. With MAP2K4/MKK4, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3.
CIViC holds 4 clinical evidence items and 0 assertions across 3 variants, naming Palbociclib, Tamoxifen and Fulvestrant. IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Stomach Adenocarcinoma.
In plain words · MAP2K7 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
MAP2K7 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signalling pathway.
No product in this corpus aims at MAP2K7 yet. Kinases are switched on by binding ATP inside the cell, so most drugs are small molecules shaped to plug that ATP pocket.
Tumour-specific alteration: the catalogues call it a tumour suppressor (IntOGen finds it knocked out more often than chance); what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA MAP2K7: RNA low tissue specificity; high antibody staining in 1 normal tissue; highest cancer staining ovarian cancer (6 of 11 high). Distribution: 3 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lung cancer (all types), Gastric & gastro-oesophageal junction cancer, Breast cancer (all types)); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt O14733; CIViC gene MAP2K7; IntOGen MAP2K7; Human Protein Atlas MAP2K7 tissue; Open Targets ENSG00000076984 associations
First described 1997. Earliest sequence paper UniProt cites for the protein: Wu et al, Mol. Cell. Biol, 1997, "Molecular cloning and characterization of human JNKK2, a novel jun NH2-terminal kinase-specific kinase". Source.
Sources: HGNC HGNC:6847 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O14733 (protein name, function text, keywords and locations (REST API)); CIViC gene MAP2K7 (4 evidence items, 0 assertions, 3 variants; diseases: Oestrogen Receptor-positive Breast Cancer, Lung Cancer (GraphQL API, CC0)); IntOGen MAP2K7 (driver in 1 cohort (Act 0, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signalling pathway. With MAP2K4/MKK4, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3. MAP2K4/MKK4 and MAP2K7/MKK7 both activate the JNKs by phosphorylation, but they differ in their preference for the phosphorylation site in the Thr-Pro-Tyr motif. MAP2K4/MKK4 shows preference for phosphorylation of the Tyr residue and MAP2K7/MKK7 for the Thr residue. The monophosphorylation of JNKs on the Thr residue is sufficient to increase JNK activity indicating that MAP2K7/MKK7 is important to trigger JNK activity, while the additional phosphorylation of the Tyr residue by MAP2K4/MKK4 ensures optimal JNK activation. Location: Nucleus; Cytoplasm (UniProt). Locus 19p13.2 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
Medium: Appendix, Bone marrow, Breast, Bronchus, Cervix, Colon, Duodenum, Endometrium.
Medium only: carcinoid, glioma, head and neck cancer, lymphoma.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"MAP2K7" OR ABSTRACT:"MAP2K7" OR TITLE:"mitogen-activated protein kinase kinase 7" OR ABSTRACT:"mitogen-activated protein kinase kinase 7" OR TITLE:"Dual specificity mitogen-activated protein kinase kinase 7" OR ABSTRACT:"Dual specificity mitogen-activated protein kinase kinase 7" OR TITLE:"MKK7" OR ABSTRACT:"MKK7" OR TITLE:"Jnkk2" OR ABSTRACT:"Jnkk2" OR TITLE:"SAPKK4" OR ABSTRACT:"SAPKK4") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about MAP2K7, not a curated reading list.