AMOT
Angiomotin
Also known as: AMOT_HUMAN, KIAA1071
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q4VCS5
- Gene
- AMOT
- Ensembl
- ENSG00000126016
- Chromosome
- X
- Canonical length
- 1084 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Cell Junctions
OverviewNCBI Gene
This gene belongs to the motin family of angiostatin binding proteins characterized by conserved coiled-coil domains and C-terminal PDZ binding motifs. The encoded protein is expressed predominantly in endothelial cells of capillaries as well as larger vessels of the placenta where it may mediate the inhibitory effect of angiostatin on tube formation and the migration of endothelial cells toward growth factors during the formation of new blood vessels. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
1084 residues, UniProt reviewed canonical sequence.
>Q4VCS5|AMOT
1 MRNSEEQPSG GTTVLQRLLQ EQLRYGNPSE NRSLLAIHQQ ATGNGPPFPS GSGNPGPQSD
61 VLSPQDHHQQ LVAHAARQEP QGQEIQSENL IMEKQLSPRM QNNEELPTYE EAKVQSQYFR
121 GQQHASVGAA FYVTGVTNQK MRTEGRPSVQ RLNPGKMHQD EGLRDLKQGH VRSLSERLMQ
181 MSLATSGVKA HPPVTSAPLS PPQPNDLYKN PTSSSEFYKA QGPLPNQHSL KGMEHRGPPP
241 EYPFKGMPPQ SVVCKPQEPG HFYSEHRLNQ PGRTEGQLMR YQHPPEYGAA RPAQDISLPL
301 SARNSQPHSP TSSLTSGGSL PLLQSPPSTR LSPARHPLVP NQGDHSAHLP RPQQHFLPNQ
361 AHQGDHYRLS QPGLSQQQQQ QQQQHHHHHH HQQQQQQQPQ QQPGEAYSAM PRAQPSSASY
421 QPVPADPFAI VSRAQQMVEI LSDENRNLRQ ELEGCYEKVA RLQKVETEIQ RVSEAYENLV
481 KSSSKREALE KAMRNKLEGE IRRMHDFNRD LRERLETANK QLAEKEYEGS EDTRKTISQL
541 FAKNKESQRE KEKLEAELAT ARSTNEDQRR HIEIRDQALS NAQAKVVKLE EELKKKQVYV
601 DKVEKMQQAL VQLQAACEKR EQLEHRLRTR LERELESLRI QQRQGNCQPT NVSEYNAAAL
661 MELLREKEER ILALEADMTK WEQKYLEENV MRHFALDAAA TVAAQRDTTV ISHSPNTSYD
721 TALEARIQKE EEEILMANKR CLDMEGRIKT LHAQIIEKDA MIKVLQQRSR KEPSKTEQLS
781 CMRPAKSLMS ISNAGSGLLS HSSTLTGSPI MEEKRDDKSW KGSLGILLGG DYRAEYVPST
841 PSPVPPSTPL LSAHSKTGSR DCSTQTERGT ESNKTAAVAP ISVPAPVAAA ATAAAITATA
901 ATITTTMVAA APVAVAAAAA PAAAAAPSPA TAAATAAAVS PAAAGQIPAA ASVASAAAVA
961 PSAAAAAAVQ VAPAAPAPVP APALVPVPAP AAAQASAPAQ TQAPTSAPAV APTPAPTPTP
1021 AVAQAEVPAS PATGPGPHRL SIPSLTCNPD KTDGPVFHSN TLERKTPIQI LGQEPDAEMV
1081 EYLILocalizationUniProt · AlphaFold · HPA
Whether an antibody against AMOT 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
- 0
- Mean surface accessibility (rSASA)
- 0.63
- Highest tissue expression
- 138 nTPM
Expression across tissuesHPA
Tissue
- epididymis: 138 nTPM
- tongue: 51 nTPM
- skeletal muscle: 37 nTPM
- seminal vesicle: 25 nTPM
- placenta: 20 nTPM
- basal ganglia: 19 nTPM
Single-cell type
- pituitary stem cells: 403 nCPM
- epididymal principal cells: 324 nCPM
- astrocytes: 94 nCPM
- myonuclei: 84 nCPM
- cytotrophoblasts: 83 nCPM
- prostatic glandular cells: 67 nCPM
Immune cell
- NK-cell: 0.3 nTPM
- MAIT T-cell: 0.2 nTPM
- gdT-cell: 0.1 nTPM
- memory CD4 T-cell: 0.1 nTPM
- memory CD8 T-cell: 0.1 nTPM
- T-reg: 0.1 nTPM
Brain region
- thalamus: 96 nTPM
- midbrain: 91 nTPM
- medulla oblongata: 87 nTPM
- hypothalamus: 86 nTPM
- amygdala: 79 nTPM
- basal ganglia: 69 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about AMOT.
Disease | GeneticClinVar
1 pathogenic / likely-pathogenic of 256 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
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)
- 0.27
- gnomAD pLI
- 1
- gnomAD missense Z
- 1.09
- DepMap mean gene effect
- 0.08
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- actin cytoskeleton organization
- angiogenesis
- blood vessel endothelial cell migration
- cell migration involved in gastrulation
- cell-cell junction assembly
- chemotaxis
- establishment of cell polarity involved in ameboidal cell migration
- gastrulation with mouth forming second
- hippo signaling
- in utero embryonic development
- intracellular protein localization
- negative regulation of angiogenesis
- negative regulation of transcription by RNA polymerase II
- negative regulation of vascular permeability
- positive regulation of blood vessel endothelial cell migration
- positive regulation of cell size
- positive regulation of embryonic development
- positive regulation of stress fiber assembly
- regulation of cell migration
- regulation of modification of postsynaptic actin cytoskeleton
- regulation of small GTPase mediated signal transduction
- vasculogenesis
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of AMOT 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 AMOT as an antibody target. Whether an autoantibody or antibody against AMOT could matter depends on whether native AMOT is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
AMOT is annotated at the cell surface, where native AMOT 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 AMOT as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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