Entity Details

Primary name TECTA_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionO75443
EntryNameTECTA_HUMAN
FullNameAlpha-tectorin
TaxID9606
Evidenceevidence at protein level
Length2155
SequenceStatuscomplete
DateCreated2004-06-07
DateModified2021-06-02

Ontological Relatives

GenesTECTA

GO terms

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GOName
GO:0005201 extracellular matrix structural constituent
GO:0005576 extracellular region
GO:0005886 plasma membrane
GO:0007160 cell-matrix adhesion
GO:0007605 sensory perception of sound
GO:0031225 anchored component of membrane
GO:0062023 collagen-containing extracellular matrix
GO:0070062 extracellular exosome

Subcellular Location

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Subcellular Location
Cell membrane
Secreted

Domains

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DomainNameCategoryType
IPR000742 EGF-like domainDomainDomain
IPR001007 VWFC domainDomainDomain
IPR001507 Zona pellucida domainDomainDomain
IPR001846 von Willebrand factor, type D domainDomainDomain
IPR002919 Trypsin Inhibitor-like, cysteine rich domainDomainDomain
IPR003886 NIDO domainDomainDomain
IPR014853 Uncharacterised domain, cysteine-richDomainDomain
IPR017977 Zona pellucida domain, conserved siteSiteConserved site
IPR025615 TILa domainDomainDomain
IPR033026 Alpha-tectorinFamilyFamily
IPR036084 Serine protease inhibitor-like superfamilyFamilyHomologous superfamily

Diseases

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Disease IDSourceNameDescription
601543 OMIMDeafness, autosomal dominant, 12 (DFNA12)A form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. The disease is caused by variants affecting the gene represented in this entry.
603629 OMIMDeafness, autosomal recessive, 21 (DFNB21)A form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. The disease is caused by variants affecting the gene represented in this entry.

Interactions

0 interactions

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