ST14
Suppressor of tumorigenicity 14 protein
Also known as: CAP3, HAI, MT-SP1, PRSS14, SNC19, ST14_HUMAN, TMPRSS14
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9Y5Y6
- Gene
- ST14
- Ensembl
- ENSG00000149418
- Chromosome
- 11
- Canonical length
- 855 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted membrane proteins, Transporters
- Subcellular location
- Nucleoplasm,Vesicles
OverviewNCBI Gene
The protein encoded by this gene is an epithelial-derived, integral membrane serine protease. This protease forms a complex with the Kunitz-type serine protease inhibitor, HAI-1, and is found to be activated by sphingosine 1-phosphate. This protease has been shown to cleave and activate hepatocyte growth factor/scattering factor, and urokinase plasminogen activator, which suggest the function of this protease as an epithelial membrane activator for other proteases and latent growth factors. The expression of this protease has been associated with breast, colon, prostate, and ovarian tumors, which implicates its role in cancer invasion, and metastasis. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
855 residues, UniProt reviewed canonical sequence.
>Q9Y5Y6|ST14
1 MGSDRARKGG GGPKDFGAGL KYNSRHEKVN GLEEGVEFLP VNNVKKVEKH GPGRWVVLAA
61 VLIGLLLVLL GIGFLVWHLQ YRDVRVQKVF NGYMRITNEN FVDAYENSNS TEFVSLASKV
121 KDALKLLYSG VPFLGPYHKE SAVTAFSEGS VIAYYWSEFS IPQHLVEEAE RVMAEERVVM
181 LPPRARSLKS FVVTSVVAFP TDSKTVQRTQ DNSCSFGLHA RGVELMRFTT PGFPDSPYPA
241 HARCQWALRG DADSVLSLTF RSFDLASCDE RGSDLVTVYN TLSPMEPHAL VQLCGTYPPS
301 YNLTFHSSQN VLLITLITNT ERRHPGFEAT FFQLPRMSSC GGRLRKAQGT FNSPYYPGHY
361 PPNIDCTWNI EVPNNQHVKV RFKFFYLLEP GVPAGTCPKD YVEINGEKYC GERSQFVVTS
421 NSNKITVRFH SDQSYTDTGF LAEYLSYDSS DPCPGQFTCR TGRCIRKELR CDGWADCTDH
481 SDELNCSCDA GHQFTCKNKF CKPLFWVCDS VNDCGDNSDE QGCSCPAQTF RCSNGKCLSK
541 SQQCNGKDDC GDGSDEASCP KVNVVTCTKH TYRCLNGLCL SKGNPECDGK EDCSDGSDEK
601 DCDCGLRSFT RQARVVGGTD ADEGEWPWQV SLHALGQGHI CGASLISPNW LVSAAHCYID
661 DRGFRYSDPT QWTAFLGLHD QSQRSAPGVQ ERRLKRIISH PFFNDFTFDY DIALLELEKP
721 AEYSSMVRPI CLPDASHVFP AGKAIWVTGW GHTQYGGTGA LILQKGEIRV INQTTCENLL
781 PQQITPRMMC VGFLSGGVDS CQGDSGGPLS SVEADGRIFQ AGVVSWGDGC AQRNKPGVYT
841 RLPLFRDWIK ENTGVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against ST14 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 1
- Mean surface accessibility (rSASA)
- 0.3
- Highest tissue expression
- 136 nTPM
Expression across tissuesHPA
Tissue
- small intestine: 136 nTPM
- duodenum: 123 nTPM
- colon: 117 nTPM
- esophagus: 108 nTPM
- stomach: 61 nTPM
- pancreas: 61 nTPM
Single-cell type
- esophageal apical cells: 547 nCPM
- colonocytes: 541 nCPM
- ocular epithelial cells: 475 nCPM
- urothelial cells: 451 nCPM
- enterocytes: 447 nCPM
- endometrial glandular cells: 340 nCPM
Immune cell
- plasmacytoid DC: 25 nTPM
- myeloid DC: 6.2 nTPM
- memory B-cell: 5.1 nTPM
- classical monocyte: 3.6 nTPM
- naive B-cell: 3.6 nTPM
- eosinophil: 3.4 nTPM
Brain region
- thalamus: 19 nTPM
- pons: 5.3 nTPM
- white matter: 4.4 nTPM
- medulla oblongata: 2.8 nTPM
- cerebral cortex: 2.7 nTPM
- cerebellum: 2.6 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about ST14.
Disease | AllUniProt
Conditions ST14 is implicated in, by any mechanism.
- Ichthyosis, congenital, autosomal recessive 11 (ARCI11) MIM:602400
Disease | GeneticClinVar
15 pathogenic / likely-pathogenic of 307 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Autosomal recessive congenital ichthyosis 11
- Ichthyosis
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.38
- gnomAD pLI
- 0.56
- gnomAD missense Z
- 1.25
- DepMap mean gene effect
- 0.07
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- epithelial cell morphogenesis involved in placental branching
- keratinocyte differentiation
- neural tube closure
- protein catabolic process
- proteolysis
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- SEA domain
- CUB domain
- Serine proteases, trypsin domain
- Low-density lipoprotein (LDL) receptor class A repeat
- Peptidase S1, PA clan
- Serine proteases, trypsin family, histidine active site
- Low-density lipoprotein (LDL) receptor class A, conserved site
- Serine proteases, trypsin family, serine active site
- Spermadhesin, CUB domain superfamily
- LDL receptor-like superfamily
- SEA domain superfamily
- Low-density lipoprotein receptor domain class A
- Trypsin
- CUB domain
- SEA domain
- Peptidase S1A, matripase
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of ST14 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads ST14 as an antibody target. Whether an autoantibody or antibody against ST14 could matter depends on whether native ST14 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ST14 is annotated at the cell surface, where native ST14 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label ST14 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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