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Protein Page:
APCL (human)
p Phosphorylation
a Acetylation
m Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
u Ubiquitination
s Sumoylation
n Neddylation
gl O-GlcNAc
ga O-GalNAc
h Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage

Overview
APCL Promotes rapid degradation of CTNNB1 and may function as a tumor suppressor. May function in Wnt signaling. Belongs to the adenomatous polyposis coli (APC) family. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Tumor suppressor; Membrane protein, peripheral
Cellular Component: Golgi membrane; microtubule cytoskeleton; Golgi apparatus; cytoplasmic microtubule; perinuclear region of cytoplasm; cytoplasm; actin filament; catenin complex
Molecular Function: protein binding; microtubule binding; beta-catenin binding
Biological Process: Wnt receptor signaling pathway
Reference #:  O95996 (UniProtKB)
Alt. Names/Synonyms: adenomatosis polyposis coli 2; adenomatous polyposis coli like; Adenomatous polyposis coli protein 2; Adenomatous polyposis coli protein-like; APC-like; APC2; APCL
Gene Symbols: APC2
Molecular weight: 243,949 Da
Basal Isoelectric point: 9.08  Predict pI for various phosphorylation states
Select Structure to View Below

APCL

Protein Structure Not Found.


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Modification Sites and Domains Show Modification Legend
Click here to view phosphorylation modifications only

Modification Sites in Parent Protein, Orthologs, and Isoforms Show Modification Legend
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       human

 
0 6 T104 GPEPAARTPEGsPVH
0 8 S108-p AARTPEGsPVHGsGP
0 2 S113-p EGsPVHGsGPSKDSF
0 2 S510-p EELHQVVssILRNLs
0 2 S511-p ELHQVVssILRNLsW
0 2 S517-p ssILRNLsWRADINS
0 1 S678-p MLRNLVHsKHKMIAM
0 2 S710 QAAATAVSPGSCVPS
0 1 S996 RVRTIKLSPTYQHVP
0 1 I1021 EPLAGPGISPGARKQ
0 2 S1052-p AAPLSVAsKALQKLA
0 1 R1331 GPAPTGSRPRGAADQ
0 1 S1585 SLSSSASSLSEPEPS
0 1 S1587 SSSASSLSEPEPSEP
0 1 A1662 TRLDERPAEGSRERG
0 1 S1665 DERPAEGSRERGEEA
0 1 S1834-p AAPAKVPsPGQQRSR
0 2 R1890 SQPLPRKRPPVTQAA
0 1 T1894 PRKRPPVTQAAGALP
0 1 S1906 ALPGPGASPVPKTPA
0 2 S2009-p PGLRRRRsELSSAES
0 1 S2025 ASAPQGASPRRGRPA
0 5 S2101 ETVKRYASLPHISVA
0 3 S2172 TALPLRGSTPEDAPA
0 3 T2173 ALPLRGSTPEDAPAG
0 1 S2203-p VAAPKTNsstsPSLE
0 1 S2204-p AAPKTNsstsPSLET
0 1 T2205-p APKTNsstsPSLETR
0 3 S2206-p PKTNsstsPSLETRE
  mouse

 
T104-p GPEPAARtPEGsPVH
S108-p AARtPEGsPVHGsGP
S113-p EGsPVHGsGPSKDSF
S503 EELHQVVSSILRNLS
S504 ELHQVVSSILRNLSW
S510 SSILRNLSWRADINS
S671 MLRNLVHSKHKMIAM
S703-p QAAAMAVsPGTCVPS
S987-p RVRTIKLsPTYQHVP
T1012-p RPLVGPGtSPGARKQ
S1043-p ASPLPIAsKVLQKLV
R1317-m2 GPAPAGSrARSATDK
S1563-p SLTSSASsLsEPEAP
S1565-p TSSASsLsEPEAPEQ
T1632-p LRSDIRPtEItQKCQ
T1635-p DIRPtEItQKCQEEV
S1805 ETVTKAPSPEQQRSR
S1861-p SQPLPRRsPLATPTG
T1865 PRRsPLATPTGGPLP
S1877 PLPGPGGSLVPKSPA
S1981-p GLLRRRRsELSSADS
S1997-p ASTSQAAsPRRGRPA
S2071-p ETVKRYAsLPHISVS
S2142-p TALPLRVssPEDSPA
S2143-p ALPLRVssPEDSPAG
S2173 VATSKTNSSTsPSLE
S2174 ATSKTNSSTsPSLES
T2175 TSKTNSSTsPSLESR
S2176-p SKTNSSTsPSLESRD
  rat

 
T104 GPEPAAQTPEGSPVH
S108 AAQTPEGSPVHGPAP
P113 EGSPVHGPAPSKDSF
S508 EELHQVVSSILRNLS
S509 ELHQVVSSILRNLSW
S515 SSILRNLSWRADINS
S676 MLRNLVHSKHKMIAM
S708 QAAAMAVSPGTCVPS
S992 RVRTIKLSPTYQHVP
T1017 RPLVGLGTSPGTRKQ
S1048 ASPLPVTSKVLQKLV
R1324 GPAPAGSRARSAADK
S1572 SLTSSASSLSEPEAS
S1574 TSSASSLSEPEASEQ
T1639 VRSDIRPTELPQKCR
P1642 DIRPTELPQKCREEV
S1812 ETATKTPSPEQQRSR
S1868 SQSLPRRSPLAtPTG
T1872-p PRRSPLAtPTGGPLP
S1884-p PLPGPGGsPVPKSPA
S1988 GLLRRRRSELSSADS
S2004 VSTSQTASPCRGRPA
S2078 ETVKRYASLPHISVS
S2149 TALPLRGSSPEDSPA
S2150 ALPLRGSSPEDSPAG
S2180 VATSKTNSSTSPSLE
S2181 ATSKTNSSTSPSLES
T2182 TSKTNSSTSPSLESR
S2183 SKTNSSTSPSLESRD
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