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PIM1 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity.
CIViC holds 5 clinical evidence items and 0 assertions across 5 variants, naming Ibrutinib. Open Targets scores its association with cancer at 0.70 (direct and indirect evidence; datatypes literature 0.99, genetic association 0.48, somatic mutation 0.83, clinical 0.12). IntOGen calls it a driver in 6 cohorts (3 activating, 3 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS, Non-Hodgkin Lymphoma, Plasma Cell Myeloma.
In plain words · PIM1 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
PIM1 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis.
No product in this corpus aims at PIM1 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 an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a tumour suppressor (IntOGen finds it knocked out more often than chance), so the direction differs between cohorts but the alteration is somatic either way; 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 PIM1: RNA tissue enhanced (bone marrow 207 nTPM); blood lineage lineage enriched (granulocytes 323 nTPM); no normal tissue stained high. Distribution: 3 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Multiple myeloma, Lung cancer (all types)); Open Targets associates it with 1 specific cancer type at or above 0.5 (diffuse large B-cell lymphoma). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P11309; CIViC gene PIM1; IntOGen PIM1; Human Protein Atlas PIM1 tissue; Open Targets ENSG00000137193 associations
First described 1987. Earliest sequence paper UniProt cites for the protein: Zakut-Houri et al, Gene, 1987, "The cDNA sequence and gene analysis of the human pim oncogene". Source.
Sources: HGNC HGNC:8986 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P11309 (protein name, function text, keywords and locations (REST API)); CIViC gene PIM1 (5 evidence items, 0 assertions, 5 variants; diseases: Diffuse Large B-cell Lymphoma Activated B-cell Type, Lung Non-small Cell Carcinoma, Diffuse Large B-cell Lymphoma (GraphQL API, CC0)); Open Targets ENSG00000137193 (association with cancer (MONDO_0004992) 0.70; per-cancer scores at or above 0.5: diffuse large B-cell lymphoma 0.65, non-Hodgkin lymphoma 0.67 (GraphQL API, CC0)); IntOGen PIM1 (driver in 6 cohorts (Act 3, LoF 3); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilisation of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signalling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, another proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Location: Cytoplasm; Nucleus; Cell membrane (UniProt). Locus 6p21.2 (HGNC).
RNA: tissue enhanced (bone marrow 207 nTPM), detected in all normal tissues. Blood: lineage enriched (granulocytes 323 nTPM).
No normal tissue stained high.
No cancer stained high; medium in urothelial cancer.
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:"PIM1" OR ABSTRACT:"PIM1" OR TITLE:"Pim-1 proto-oncogene, serine/threonine kinase" OR ABSTRACT:"Pim-1 proto-oncogene, serine/threonine kinase" OR TITLE:"Serine/threonine-protein kinase pim-1" OR ABSTRACT:"Serine/threonine-protein kinase pim-1") 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 PIM1, not a curated reading list.