Loading
APH1B (Gamma-secretase subunit APH-1B) is a gene. The public catalogues list it as a drug target, and an approved or late-stage drug is recorded against it. Tied to Desmoid tumour.
Probable subunit of the gamma-secretase complex, an endoprotease complex that catalyses the intramembrane cleavage of integral proteins such as Notch receptors and APP (amyloid-beta precursor protein). It probably represents a stabilising cofactor for the presenilin homodimer that promotes the formation of a stable complex. Probably present in a minority of gamma-secretase complexes compared to APH1A.
In plain words · APH1B (Gamma-secretase subunit APH-1B) is a gene. The public catalogues list it as a drug target, and an approved or late-stage drug is recorded against it. Tied to Desmoid tumour.
APH1B (Gamma-secretase subunit APH-1B) is a gene. The public catalogues list it as a drug target, and an approved or late-stage drug is recorded against it. Tied to Desmoid tumour.
Probable subunit of the gamma-secretase complex, an endoprotease complex that catalyses the intramembrane cleavage of integral proteins such as Notch receptors and APP (amyloid-beta precursor protein).
No product in this corpus aims at APH1B yet. Drugs bind the molecule precisely: to switch it off, flag the cell for the immune system, or deliver a payload.
Specificity not established: no corpus medicine is aimed at it and the catalogues give it only the role drug-target; HPA finds the RNA tissue enriched, which says where the protein sits but not whether the tumour differs from normal tissue. HPA APH1B: RNA tissue enriched (testis 111 nTPM); no normal tissue stained high. Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Sarcomas (soft tissue, bone, GIST)); Open Targets associates it with 1 specific cancer type at or above 0.5 (desmoid tumor). (No rule of scripts/fetch-target-specificity.ts fired.)
Sources: Human Protein Atlas APH1B tissue; Open Targets ENSG00000138613 associations
First described 2001. Earliest sequence paper UniProt cites for the protein: Wiemann et al, Genome Res, 2001, "Towards a catalog of human genes and proteins: sequencing and analysis of 500 novel complete protein coding human cDNAs". Source.
Sources: HGNC HGNC:24080 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q8WW43 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000138613 (per-cancer scores at or above 0.5: desmoid tumour 0.50 (GraphQL API, CC0))
Probable subunit of the gamma-secretase complex, an endoprotease complex that catalyses the intramembrane cleavage of integral proteins such as Notch receptors and APP (amyloid-beta precursor protein). It probably represents a stabilising cofactor for the presenilin homodimer that promotes the formation of a stable complex. Probably present in a minority of gamma-secretase complexes compared to APH1A. Location: Membrane (UniProt). Locus 15q22.2 (HGNC).
RNA: tissue enriched (testis 111 nTPM), detected in all normal tissues.
No normal tissue stained high.
No cancer sample stained medium or high.
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:"APH1B" OR ABSTRACT:"APH1B" OR TITLE:"aph-1B gamma-secretase subunit" OR ABSTRACT:"aph-1B gamma-secretase subunit" OR TITLE:"Gamma-secretase subunit APH-1B" OR ABSTRACT:"Gamma-secretase subunit APH-1B" OR TITLE:"APH-1B" OR ABSTRACT:"APH-1B" OR TITLE:"DKFZp564D0372" OR ABSTRACT:"DKFZp564D0372") 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 APH1B, not a curated reading list.
Shares Desmoid tumour, Open Targets Platform.
Shares Desmoid tumour, Open Targets Platform.
Shares Desmoid tumour, Open Targets Platform.
Shares Desmoid tumour, Open Targets Platform.