ATP1A1 (Sodium/potassium-transporting ATPase subunit alpha-1) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target and an oncogene driver, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Breast cancer, Gastric & gastro-oesophageal junction cancer and Colorectal cancer.
Catalytic subunit of the Na(+)/K(+)-ATPase pump that hydrolyses ATP to exchange ions across the plasma membrane, exporting 3 Na(+) and importing 2 K(+) per cycle against electrochemical gradients. It undergoes ATP-driven conformational changes that allow alternating binding and release of Na(+) and K(+) ions across the membrane. This process maintains essential Na(+) and K(+) gradients for membrane potential and cellular function.
Open Targets scores its association with cancer at 0.67 (direct and indirect evidence; datatypes clinical 0.18, affected pathway 0.32, literature 0.95, genetic association 0.00, somatic mutation 0.77). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Invasive Breast Carcinoma.
In plain words · ATP1A1 (Sodium/potassium-transporting ATPase subunit alpha-1) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target and an oncogene driver, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Breast cancer, Gastric & gastro-oesophageal junction cancer and Colorectal cancer.
ATP1A1 (Sodium/potassium-transporting ATPase subunit alpha-1) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target and an oncogene driver, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Breast cancer, Gastric & gastro-oesophageal junction cancer and Colorectal cancer.
Catalytic subunit of the Na(+)/K(+)-ATPase pump that hydrolyses ATP to exchange ions across the plasma membrane, exporting 3 Na(+) and importing 2 K(+) per cycle against electrochemical gradients.
No product in this corpus aims at ATP1A1 yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated 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 ATP1A1: RNA tissue enhanced (parathyroid gland 1,394 nTPM); high antibody staining in 19 normal tissues; highest cancer staining colorectal cancer (12 of 12 high). Distribution: 3 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Breast cancer (all types), Gastric & gastro-oesophageal junction cancer, Colorectal cancer); Open Targets associates it with 1 specific cancer type at or above 0.5 (aldosterone-producing adrenal cortex adenoma). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P05023; IntOGen ATP1A1; Human Protein Atlas ATP1A1 tissue; Open Targets ENSG00000163399 associations
First described 1986. Earliest sequence paper UniProt cites for the protein: Kawakami et al, J. Biochem, 1986, "Primary structure of the alpha-subunit of human Na,K-ATPase deduced from cDNA sequence". Source.
Sources: HGNC HGNC:799 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P05023 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000163399 (association with cancer (MONDO_0004992) 0.67; per-cancer scores at or above 0.5: colorectal cancer 0.50, gastric cancer 0.51 (GraphQL API, CC0)); IntOGen ATP1A1 (driver in 1 cohort (Act 1, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Catalytic subunit of the Na(+)/K(+)-ATPase pump that hydrolyses ATP to exchange ions across the plasma membrane, exporting 3 Na(+) and importing 2 K(+) per cycle against electrochemical gradients. It undergoes ATP-driven conformational changes that allow alternating binding and release of Na(+) and K(+) ions across the membrane. This process maintains essential Na(+) and K(+) gradients for membrane potential and cellular function. Could also be part of an osmosensory signalling pathway that senses body-fluid sodium levels and controls salt intake behaviour as well as voluntary water intake to regulate sodium homeostasis. Location: Cell membrane; Basolateral cell membrane; Cell membrane, sarcolemma; Cell projection, axon (UniProt). Locus 1p13.1 (HGNC).
RNA: tissue enhanced (parathyroid gland 1,394 nTPM), detected in all normal tissues.
Medium: Bronchus, Cerebral cortex, Cervix, Endometrium, Epididymis, Fallopian tube, Liver, Testis.
HPA ATP1A1 tissue · HPA ATP1A1 pathology · HPA protein class: Essential proteins, FDA approved drug targets
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:"ATP1A1" OR ABSTRACT:"ATP1A1" OR TITLE:"ATPase Na+/K+ transporting subunit alpha 1" OR ABSTRACT:"ATPase Na+/K+ transporting subunit alpha 1" OR TITLE:"Sodium/potassium-transporting ATPase subunit alpha-1" OR ABSTRACT:"Sodium/potassium-transporting ATPase subunit alpha-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 ATP1A1, not a curated reading list.