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Protein Page:
RB1CC1 (human)
p Phosphorylation
ac Acetylation
me Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
ub Ubiquitination
sm Sumoylation
ne Neddylation
gl O-GlcNAc
ga O-GalNAc
pa Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage
sc Succinylation

Overview
RB1CC1 a putative transcription factor that functions as a key regulator of Rb expression. Required for autophagosome formation. Contains a nuclear localization signal, a leucine zipper motif and a coiled-coil structure. Thought to play a biological role in controlling cell growth and progression of various cancers. Probably involved in the tumorigenesis of breast cancer. It is frequently mutated in breast cancer and shows characteristics of a classical tumor suppressor gene. Plays a crucial role in muscular differentiation and required for myogenic differentiation. Part of a complex consisting of ATG13, ULK1 and RB1CC1. This complex associates with ATG101. Under starvation conditions, is localized to phagophores. Expression levels correlated closely with those of RB1 in cancer cell lines as well as in various normal human tissues. Abundantly expressed in human musculoskeletal and cultured osteosarcoma cells. Expression was difficult to detect in immature proliferating chondroblasts or myogenic cells in embryos, but became obvious and prominent concomitantly with the maturation of osteocytes, chondrocytes, and skeletal muscle cells. Expression in these musculoskeletal cells increased with RB1 expression, which is linked to the terminal differentiation of many tissues and cells. The introduction of the wild-type protein decreased the formation of macroscopic colonies in a cell growth assay. Note: This description may include information from UniProtKB.
Protein type: Transcription factor; Autophagy; DNA binding protein
Cellular Component: nuclear membrane; pre-autophagosomal structure membrane; cytoplasm; cytosol
Molecular Function: protein binding; protein kinase binding
Biological Process: positive regulation of cell size; transcription, DNA-dependent; regulation of transcription, DNA-dependent; heart development; JNK cascade; regulation of autophagy; positive regulation of protein amino acid phosphorylation; liver development; cell cycle; negative regulation of apoptosis; autophagic vacuole formation
Reference #:  Q8TDY2 (UniProtKB)
Alt. Names/Synonyms: 200 kDa FAK family kinase-interacting protein; CC1; FIP200; KIAA0203; RB1-inducible coiled-coil 1; RB1-inducible coiled-coil protein 1; RB1CC1; RBCC1; RBICC
Gene Symbols: RB1CC1
Molecular weight: 183,091 Da
Basal Isoelectric point: 5.3  Predict pI for various phosphorylation states
CST Pathways:  Autophagy Signaling
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
Select Structure to View Below

RB1CC1

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 2 S105-p MEIKVEEsLMMPAVF
0 1 T114 MMPAVFHTVASRTQL
0 1 S117 AVFHTVASRTQLALE
0 1 S134-p EVAKKLCsFCEGLVH
0 3 K201 TAVSVMAKIPLLECL
0 54 S222-p ECLGRLDsLPEHEDs
0 1 S229-p sLPEHEDsEKAEMKR
0 8 S237-p EKAEMKRstELVLsP
0 8 T238-p KAEMKRstELVLsPD
0 14 S243-p RstELVLsPDMPRTT
0 1 E252 DMPRTTNEsLLtsFP
0 3 S253-p MPRTTNEsLLtsFPK
0 2 T256-p TTNEsLLtsFPKsVE
0 15 S257-p TNEsLLtsFPKsVEH
0 7 S261-p LLtsFPKsVEHVsPD
0 2 S266-p PKsVEHVsPDTADAE
0 1 A270 EHVsPDTADAESGKE
0 1 K387 GRLVNEQKELAQGFL
0 1 S490-p VKIVEALsTVPQMYC
0 1 K522 EWAGALVKDGKRLYE
0 1 S537-p AEKSKREsFGKLFRK
0 4 S624-p NLVKAAQsLDEMsQT
0 1 S629-p AQsLDEMsQTItDLL
0 1 T633-p DEMsQTItDLLSEQK
0 5 S644-p SEQKASVsQTsPQsA
0 13 S647-p KASVsQTsPQsAssP
0 6 S650-p VsQTsPQsAssPRME
0 2 S652-p QTsPQsAssPRMEST
0 13 S653-p TsPQsAssPRMESTA
0 1 T664-p ESTAGITtTTSPRTP
0 1 T666 TAGITtTTSPRTPPP
0 1 S667 AGITtTTSPRTPPPL
0 1 K883-ac GKLDGLIkETEENEN
0 1 K891-ac ETEENENkIKKLKGE
0 1 C901 KLKGELVCLEEVLQN
0 2 K930 VICLQNEKDQKLLEM
0 1 K952 NCEIKELKQSREIVL
0 1 K963 EIVLEDLKKLHVEND
0 1 S986-p ELQSLEQsHLKELED
0 1 S1091 QQKETLKSLLEQETE
0 1 Y1205-p ITQQEEKyEAIIQNL
0 1 S1222-p DRQKLVSsQEQDREQ
0 1 K1263-ac VEKELLEkVKHLENQ
0 1 S1274-p LENQIAKsPAIDSTR
0 1 S1286 STRGDSSSLVAELQE
0 3 K1343 LTREKMRKENIINDL
0 3 K1353 IINDLSDKLKSTMQQ
0 2 S1370-p RDKDLIEsLSEDRAR
0 1 K1456 IHMLSEEKQRIMLLE
0 3 S1482-p RLNQRLMsQsMSSVS
0 3 S1484-p NQRLMsQsMSSVSSR
  mouse

 
S105-p MEIKVEEsLMMPAVF
T114-p MMPAVFHtVAsRTQL
S117-p AVFHtVAsRTQLAVE
S134 DVAKKLCSFCEGLVH
K201-ac TAVSVMAkIPLLECL
S222-p ECLGRPDsLNEHEGS
S229 sLNEHEGSEKAEMKR
S237-p EKAEMKRstELVLsP
T238-p KAEMKRstELVLsPD
S243-p RstELVLsPDMPRTT
T252-p DMPRTTNtsLVtsFH
S253-p MPRTTNtsLVtsFHK
T256-p TTNtsLVtsFHKsME
S257-p TNtsLVtsFHKsMEH
S261-p LVtsFHKsMEHVAPD
A266 HKsMEHVAPDPtGTE
T270-p EHVAPDPtGTERGKE
K386-ub SRLVNEQkELAQGFL
S489 VRIVEALSTVPQMYC
K521-ac EWAGALVkDGKQLYE
S536 AEKSKRESFGKLFRK
S623-p NLVKAAQsLDEMsQT
S628-p AQsLDEMsQTITDLL
T632 DEMsQTITDLLNEQK
S643-p NEQKVSTsQAsPQsA
S646-p KVSTsQAsPQsAAsP
S649-p TsQAsPQsAAsPRIE
A651 QAsPQsAAsPRIEST
S652-p AsPQsAAsPRIESTT
T663 ESTTGITTTtSPKTP
T665-p TTGITTTtSPKTPPP
S666 TGITTTtSPKTPPPL
K882 CKLDALVKDSEENVN
K890 DSEENVNKILKLKEN
S900-p KLKENLVsLEEALQN
K929-ac IVCVQQEkDQKLLEM
K951-ac HCEIKELkQSREMAL
K962-ac EMALEDLkKLHDEKI
N982 EFQCLEQNHLKELED
S1087-p QQKEMLKsLLEQETE
Y1201 ITQQEEKYEALIQNL
N1218 DKERLVKNHEQDKEH
K1259 VEKELLEKVKHLENQ
T1270 LENQIAKTPAFESAR
S1282-p SAREDSSsLVAELQE
K1339-ac LTREKMRkENIINDL
K1349-ac IINDLSDkLKSTMQQ
S1366-p RDKDLIEsLSEDRAR
K1450-ac ENMLSEEkQRIMLLE
S1476 RLNQRLMSQsLSSVS
S1478-p NQRLMSQsLSSVSSR
  rat

 
S105 MEIKVEESLMMPAVF
T114 MMPAVFHTVASRTQL
S117 AVFHTVASRTQLAVE
S134 EVAKKLCSFCEGLVH
K201 TAVSVMAKIPLLECL
S222 ECLGRPDSLNEHEGS
S229 SLNEHEGSEKADMKR
S237-p EKADMKRsTELVLSP
T238 KADMKRsTELVLSPD
S243 RsTELVLSPDMPRTT
T252 DMPRTTNTSLLTSFH
S253 MPRTTNTSLLTSFHK
T256 TTNTSLLTSFHKSVE
S257 TNTSLLTSFHKSVEH
S261 LLTSFHKSVEHVAPD
A266 HKSVEHVAPDVTDAE
T270 EHVAPDVTDAEQGKE
K386 SRLVNEQKELAQGFL
S489 VRIVEALSTVPQMYC
K521 EWAGALVKDGKQLYE
S536 AEKSKRESFGKLFRK
S623 NLVKAAQSLDEMSQT
S628 AQSLDEMSQTITDLL
T632 DEMSQTITDLLNEQK
S643 NEQKVSTSQASPQSA
S646 KVSTSQASPQSAASP
S649 TSQASPQSAASPRIE
A651 QASPQSAASPRIEST
S652 ASPQSAASPRIESTT
T663 ESTTGITTTTsPKAP
T665 TTGITTTTsPKAPPP
S666-p TGITTTTsPKAPPPL
K882 CKLNTLEKDSEENVN
K890 DSEENVNKILKLKED
S900 KLKEDLVSLEEALQN
K929 IVCMQHEKDQKLLEM
K951 NSEIKELKQSREMVL
K962 EMVLEDLKKLHDEKI
N982 EFQCLEQNHLKELED
S1087 QQKETLKSLLEQETE
Y1201 ITQQEEKYKALIQNL
N1218 DKQRLAMNHEQDKEQ
K1259 VEKELLEKVKHLENQ
S1270 LENQIAKSPAFESAR
S1282 SAREDSSSLVAELQE
K1339 LTREKMRKENIINDL
K1349 IINDLSDKLKSTMQQ
S1366 RDKDLIESLSEDRAR
K1450 ENMLSEEKQRIMLLE
S1476 RLNQRLMSQSLSSVS
S1478 NQRLMSQSLSSVSSR
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