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INPPL1 (Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Endometrial cancer.
Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyses the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways. Required for correct mitotic spindle orientation and therefore progression of mitosis. Plays a central role in regulation of PI3K-dependent insulin signalling, although the precise molecular mechanisms and signalling pathways remain unclear.
IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Endometrial Carcinoma.
In plain words · INPPL1 (Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Endometrial cancer.
INPPL1 (Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Endometrial cancer.
Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyses the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways.
No product in this corpus aims at INPPL1 yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
First described 1995. Earliest sequence paper UniProt cites for the protein: Hejna J.A. et al, Genomics, 1995, "Cloning and characterization of a human cDNA (INPPL1) sharing homology with inositol polyphosphate phosphatases". Source.
Sources: HGNC HGNC:6080 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O15357 (protein name, function text, keywords and locations (REST API)); IntOGen INPPL1 (driver in 1 cohort (Act 0, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyses the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways. Required for correct mitotic spindle orientation and therefore progression of mitosis. Plays a central role in regulation of PI3K-dependent insulin signalling, although the precise molecular mechanisms and signalling pathways remain unclear. While overexpression reduces both insulin-stimulated MAP kinase and Akt activation, its absence does not affect insulin signalling or GLUT4 trafficking. Confers resistance to dietary obesity. May act by regulating AKT2, but not AKT1, phosphorylation at the plasma membrane. Location: Cytoplasm, cytosol; Cytoplasm, cytoskeleton; Membrane; Cell projection, filopodium (UniProt). Locus 11q13.4 (HGNC).
Query for this target: (TITLE:"INPPL1" OR ABSTRACT:"INPPL1" OR TITLE:"inositol polyphosphate phosphatase like 1" OR ABSTRACT:"inositol polyphosphate phosphatase like 1" OR TITLE:"Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2" OR ABSTRACT:"Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2" OR TITLE:"SHIP2" OR ABSTRACT:"SHIP2") 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 INPPL1, not a curated reading list.