APC
Adenomatous polyposis coli protein
Also known as: APC_HUMAN, DP2, DP2.5, DP3, PPP1R46
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P25054
- Gene
- APC
- Ensembl
- ENSG00000134982
- Chromosome
- 5
- Canonical length
- 2843 aa
- Protein class
- Cancer-related genes, Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Golgi apparatus,Plasma membrane
- Quaternary structure
- Homooligomer
OverviewNCBI Gene
This gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in other processes including cell migration and adhesion, transcriptional activation, and apoptosis. Defects in this gene cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy. Mutations in the APC gene have been found to occur in most colorectal cancers, where disease-associated mutations tend to be clustered in a small region designated the mutation cluster region (MCR) and result in a truncated protein product. [provided by RefSeq, Jun 2022]
Canonical amino-acid sequenceUniProt
2843 residues, UniProt reviewed canonical sequence.
>P25054|APC
1 MAAASYDQLL KQVEALKMEN SNLRQELEDN SNHLTKLETE ASNMKEVLKQ LQGSIEDEAM
61 ASSGQIDLLE RLKELNLDSS NFPGVKLRSK MSLRSYGSRE GSVSSRSGEC SPVPMGSFPR
121 RGFVNGSRES TGYLEELEKE RSLLLADLDK EEKEKDWYYA QLQNLTKRID SLPLTENFSL
181 QTDMTRRQLE YEARQIRVAM EEQLGTCQDM EKRAQRRIAR IQQIEKDILR IRQLLQSQAT
241 EAERSSQNKH ETGSHDAERQ NEGQGVGEIN MATSGNGQGS TTRMDHETAS VLSSSSTHSA
301 PRRLTSHLGT KVEMVYSLLS MLGTHDKDDM SRTLLAMSSS QDSCISMRQS GCLPLLIQLL
361 HGNDKDSVLL GNSRGSKEAR ARASAALHNI IHSQPDDKRG RREIRVLHLL EQIRAYCETC
421 WEWQEAHEPG MDQDKNPMPA PVEHQICPAV CVLMKLSFDE EHRHAMNELG GLQAIAELLQ
481 VDCEMYGLTN DHYSITLRRY AGMALTNLTF GDVANKATLC SMKGCMRALV AQLKSESEDL
541 QQVIASVLRN LSWRADVNSK KTLREVGSVK ALMECALEVK KESTLKSVLS ALWNLSAHCT
601 ENKADICAVD GALAFLVGTL TYRSQTNTLA IIESGGGILR NVSSLIATNE DHRQILRENN
661 CLQTLLQHLK SHSLTIVSNA CGTLWNLSAR NPKDQEALWD MGAVSMLKNL IHSKHKMIAM
721 GSAAALRNLM ANRPAKYKDA NIMSPGSSLP SLHVRKQKAL EAELDAQHLS ETFDNIDNLS
781 PKASHRSKQR HKQSLYGDYV FDTNRHDDNR SDNFNTGNMT VLSPYLNTTV LPSSSSSRGS
841 LDSSRSEKDR SLERERGIGL GNYHPATENP GTSSKRGLQI STTAAQIAKV MEEVSAIHTS
901 QEDRSSGSTT ELHCVTDERN ALRRSSAAHT HSNTYNFTKS ENSNRTCSMP YAKLEYKRSS
961 NDSLNSVSSS DGYGKRGQMK PSIESYSEDD ESKFCSYGQY PADLAHKIHS ANHMDDNDGE
1021 LDTPINYSLK YSDEQLNSGR QSPSQNERWA RPKHIIEDEI KQSEQRQSRN QSTTYPVYTE
1081 STDDKHLKFQ PHFGQQECVS PYRSRGANGS ETNRVGSNHG INQNVSQSLC QEDDYEDDKP
1141 TNYSERYSEE EQHEEEERPT NYSIKYNEEK RHVDQPIDYS LKYATDIPSS QKQSFSFSKS
1201 SSGQSSKTEH MSSSSENTST PSSNAKRQNQ LHPSSAQSRS GQPQKAATCK VSSINQETIQ
1261 TYCVEDTPIC FSRCSSLSSL SSAEDEIGCN QTTQEADSAN TLQIAEIKEK IGTRSAEDPV
1321 SEVPAVSQHP RTKSSRLQGS SLSSESARHK AVEFSSGAKS PSKSGAQTPK SPPEHYVQET
1381 PLMFSRCTSV SSLDSFESRS IASSVQSEPC SGMVSGIISP SDLPDSPGQT MPPSRSKTPP
1441 PPPQTAQTKR EVPKNKAPTA EKRESGPKQA AVNAAVQRVQ VLPDADTLLH FATESTPDGF
1501 SCSSSLSALS LDEPFIQKDV ELRIMPPVQE NDNGNETESE QPKESNENQE KEAEKTIDSE
1561 KDLLDDSDDD DIEILEECII SAMPTKSSRK AKKPAQTASK LPPPVARKPS QLPVYKLLPS
1621 QNRLQPQKHV SFTPGDDMPR VYCVEGTPIN FSTATSLSDL TIESPPNELA AGEGVRGGAQ
1681 SGEFEKRDTI PTEGRSTDEA QGGKTSSVTI PELDDNKAEE GDILAECINS AMPKGKSHKP
1741 FRVKKIMDQV QQASASSSAP NKNQLDGKKK KPTSPVKPIP QNTEYRTRVR KNADSKNNLN
1801 AERVFSDNKD SKKQNLKNNS KVFNDKLPNN EDRVRGSFAF DSPHHYTPIE GTPYCFSRND
1861 SLSSLDFDDD DVDLSREKAE LRKAKENKES EAKVTSHTEL TSNQQSANKT QAIAKQPINR
1921 GQPKPILQKQ STFPQSSKDI PDRGAATDEK LQNFAIENTP VCFSHNSSLS SLSDIDQENN
1981 NKENEPIKET EPPDSQGEPS KPQASGYAPK SFHVEDTPVC FSRNSSLSSL SIDSEDDLLQ
2041 ECISSAMPKK KKPSRLKGDN EKHSPRNMGG ILGEDLTLDL KDIQRPDSEH GLSPDSENFD
2101 WKAIQEGANS IVSSLHQAAA AACLSRQASS DSDSILSLKS GISLGSPFHL TPDQEEKPFT
2161 SNKGPRILKP GEKSTLETKK IESESKGIKG GKKVYKSLIT GKVRSNSEIS GQMKQPLQAN
2221 MPSISRGRTM IHIPGVRNSS SSTSPVSKKG PPLKTPASKS PSEGQTATTS PRGAKPSVKS
2281 ELSPVARQTS QIGGSSKAPS RSGSRDSTPS RPAQQPLSRP IQSPGRNSIS PGRNGISPPN
2341 KLSQLPRTSS PSTASTKSSG SGKMSYTSPG RQMSQQNLTK QTGLSKNASS IPRSESASKG
2401 LNQMNNGNGA NKKVELSRMS STKSSGSESD RSERPVLVRQ STFIKEAPSP TLRRKLEESA
2461 SFESLSPSSR PASPTRSQAQ TPVLSPSLPD MSLSTHSSVQ AGGWRKLPPN LSPTIEYNDG
2521 RPAKRHDIAR SHSESPSRLP INRSGTWKRE HSKHSSSLPR VSTWRRTGSS SSILSASSES
2581 SEKAKSEDEK HVNSISGTKQ SKENQVSAKG TWRKIKENEF SPTNSTSQTV SSGATNGAES
2641 KTLIYQMAPA VSKTEDVWVR IEDCPINNPR SGRSPTGNTP PVIDSVSEKA NPNIKDSKDN
2701 QAKQNVGNGS VPMRTVGLEN RLNSFIQVDA PDQKGTEIKP GQNNPVPVSE TNESSIVERT
2761 PFSSSSSSKH SSPSGTVAAR VTPFNYNPSP RKSSADSTSA RPSQIPTPVN NNTKKRDSKT
2821 DSTESSGTQS PKRHSGSYLV TSVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against APC 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
- Highest tissue expression
- 39 nTPM
Expression across tissuesHPA
Tissue
- amygdala: 39 nTPM
- cerebral cortex: 35 nTPM
- hippocampal formation: 34 nTPM
- midbrain: 21 nTPM
- retina: 19 nTPM
- basal ganglia: 16 nTPM
Single-cell type
- astrocytes: 739 nCPM
- bergmann glia: 720 nCPM
- ependymal cells: 304 nCPM
- neutrophils: 302 nCPM
- retinal bipolar cells: 296 nCPM
- oligodendrocyte progenitor cells: 242 nCPM
Immune cell
- basophil: 12 nTPM
- neutrophil: 11 nTPM
- eosinophil: 4.9 nTPM
- naive B-cell: 3.1 nTPM
- gdT-cell: 2.9 nTPM
- memory B-cell: 2.9 nTPM
Brain region
- hippocampal formation: 160 nTPM
- thalamus: 131 nTPM
- pons: 130 nTPM
- midbrain: 117 nTPM
- cerebral cortex: 112 nTPM
- amygdala: 110 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about APC.
Disease | AllUniProt
Conditions APC is implicated in, by any mechanism.
- Familial adenomatous polyposis 1 (FAP1) MIM:175100
- Desmoid disease, hereditary (DESMD) MIM:135290
- Medulloblastoma (MDB) MIM:155255
- Gastric cancer (GASC) MIM:613659
- Hepatocellular carcinoma (HCC) MIM:114550
- Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) MIM:619182
Disease | GeneticClinVar
2,615 pathogenic / likely-pathogenic of 16,882 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Familial adenomatous polyposis 1
- Hereditary cancer-predisposing syndrome
- Familial multiple polyposis syndrome
- Carcinoma of colon
- Classic or attenuated familial adenomatous polyposis
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)
- 0.16
- gnomAD pLI
- 1
- gnomAD missense Z
- 0.17
- DepMap mean gene effect
- -0.32
- DepMap dependency class
- selective
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
- bicellular tight junction assembly
- cell adhesion
- cell fate specification
- cell migration
- DNA damage response
- endocardial cushion morphogenesis
- heart valve development
- insulin receptor signaling pathway
- mitotic cytokinesis
- mitotic spindle assembly checkpoint signaling
- negative regulation of canonical Wnt signaling pathway
- negative regulation of cell cycle G1/S phase transition
- negative regulation of cell population proliferation
- negative regulation of cyclin-dependent protein serine/threonine kinase activity
- negative regulation of G1/S transition of mitotic cell cycle
- negative regulation of microtubule depolymerization
- nervous system development
- pattern specification process
- positive regulation of apoptotic process
- positive regulation of cell migration
- positive regulation of cold-induced thermogenesis
- positive regulation of protein catabolic process
- positive regulation of protein localization to centrosome
- positive regulation of pseudopodium assembly
- proteasome-mediated ubiquitin-dependent protein catabolic process
- protein-containing complex assembly
- regulation of attachment of spindle microtubules to kinetochore
- regulation of microtubule-based movement
- regulation of microtubule-based process
- Wnt signaling pathway
Molecular functions
- beta-catenin binding
- dynein complex binding
- gamma-catenin binding
- microtubule binding
- microtubule plus-end binding
- protein kinase binding
- protein kinase regulator activity
- ubiquitin protein ligase binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Armadillo
- Adenomatous polyposis coli protein repeat
- SAMP
- Adenomatous polyposis coli protein basic domain
- Armadillo-like helical
- Armadillo-type fold
- Adenomatous polyposis coli (APC) family
- Adenomatous polyposis coli protein
- Adenomatous polyposis coli, N-terminal dimerisation domain
- APC, N-terminal coiled-coil domain superfamily
- Adenomatous polyposis coli (APC) repeat
- Armadillo/beta-catenin-like repeat
- APC repeat
- SAMP Motif
- APC basic domain
- Adenomatous polyposis coli tumour suppressor protein
- Armadillo-associated region on APC
- Coiled-coil N-terminus of APC, dimerisation domain
- Adenomatous polyposis coli (APC) repeat
- EB-1 binding
- Adenomatous polyposis coli protein, 15 residue repeat
- EB-1 Binding Domain
- APC 15 residue motif
- Unstructured region on APC between 1st and 2nd catenin-bdg motifs
- Unstructured region on APC between 1st two creatine-rich regions
- Unstructured region on APC between APC_crr and SAMP
- Unstructured region on APC between SAMP and APC_crr
- Unstructured region on APC between APC_crr regions 5 and 6
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of APC 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 APC as an antibody target. Whether an autoantibody or antibody against APC could matter depends on whether native APC is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
APC is annotated at the cell surface, where native APC 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 APC as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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