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Protein Page:
GRK2 (mouse)
p Phosphorylation
ac Acetylation
me Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
ub Ubiquitylation
sm Sumoylation
ne Neddylation
gl O-GlcNAc
ga O-GalNAc
pa Palmitoylation
ad Adenylation
sn S-Nitrosylation
ca Caspase cleavage
sc Succinylation

Overview
GRK2 a ubiquitous protein kinase of the GRK family. Phosphorylates the beta-2-adrenergic receptor and related G-protein-coupled receptors. Appears to mediate agonist-specific desensitization observed at high agonist concentrations. Expression level is consistently elevated in chronic human heart failure. Mouse models of severe heart failure have been used to demonstrate that inhibition of BARK1 with a peptide inhibitor is sufficient to increase mean survival, reduce dialation and improve cardiac function. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 2.7.11.15; Protein kinase, AGC; AGC group; GRK family; BARK subfamily
Cellular Component: apical plasma membrane; axon; basolateral plasma membrane; caveola; cytoplasm; dendritic shaft; dendritic spine; membrane; synapse
Molecular Function: beta-adrenergic receptor kinase activity; Edg-2 lysophosphatidic acid receptor binding; G-protein coupled receptor kinase activity; protein binding; protein kinase activity; protein serine/threonine kinase activity
Biological Process: cardiac muscle contraction; desensitization of G-protein coupled receptor protein signaling pathway; entry of virus into host cell; follicle-stimulating hormone signaling pathway; G-protein coupled receptor protein signaling pathway; heart development; negative regulation of G-protein coupled receptor protein signaling pathway; negative regulation of striated muscle contraction; negative regulation of the force of heart contraction by chemical signal; peptidyl-serine phosphorylation; peptidyl-threonine phosphorylation; positive regulation of catecholamine secretion; protein amino acid phosphorylation; receptor internalization; regulation of the force of heart contraction; response to organic cyclic substance; response to oxidative stress; tachykinin signaling pathway; viral genome replication
Reference #:  Q99MK8 (UniProtKB)
Alt. Names/Synonyms: Adrbk-1; Adrbk1; adrenergic receptor kinase, beta 1; ARBK1; Bark-1; beta ARK; beta ARK1; Beta-adrenergic receptor kinase 1; beta-adrenergic receptor kinase-1; beta-AR kinase-1; Beta-ARK-1; betaARK1; G-protein-coupled receptor kinase 2; Grk2
Gene Symbols: Adrbk1
Molecular weight: 79,639 Da
Basal Isoelectric point: 6.89  Predict pI for various phosphorylation states
CST Pathways:  GPCR Signaling to MAPKs
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
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GRK2

Protein Structure Not Found.
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Substrate Sequence Logo
Sequence Logo

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Sites Implicated In
cell motility, altered: Y13‑p, Y86‑p, Y92‑p, S670‑p
molecular association, regulation: S670‑p

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



 LTP 

LTP: 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.


 HTP 

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


       mouse

 
5 0 Y13‑p AVLADVSyLMAMEKS
2 0 S29 ATPAARASKKILLPE
0 1 T54 LEDRGEVTFEKIFSQ
0 1 K57 RGEVTFEKIFSQKLG
0 4 K62 FEKIFSQKLGYLLFR
5 0 Y86‑p AKPLVEFyEEIKKyE
5 0 Y92‑p FyEEIKKyEKLETEE
0 1 K126 ACSHPFSKNATEHVQ
0 1 K170 QKFIESDKFTRFCQW
0 1 S247 RIMLSLVSTGDCPFI
0 1 T248 IMLSLVSTGDCPFIV
0 1 T263 CMSYAFHTPDKLSFI
0 1 K319 FVVYRDLKPANILLD
0 4 K344‑ub GLACDFSkKRPHASV
0 1 K345 LACDFSkKRPHASVG
0 71 Y356‑p ASVGTHGyMAPEVLQ
0 1 S416 MAVELPDSFSPELRS
0 1 K448 GRGAQEVKESPFFRS
0 3 S487‑p ADAFDIGsFDEEDTK
0 1 S501 KGIKLLDSDQELYRN
0 1 Y506 LDSDQELYRNFPLTI
0 1 K628 LLKIRGGKQFVLQCD
0 1 K644 DPELVQWKKELRDAY
3 45 S670‑p KMKNKPRsPVVELsK
0 2 S676‑p RsPVVELsKVPLIQR
0 2 K677 sPVVELsKVPLIQRG
2 9 S685 VPLIQRGSANGL___
  human

 
Y13‑p AVLADVSyLMAMEKS
S29‑p ATPAARAsKKILLPE
T54‑p LEDRGEVtFEkIFSQ
K57‑ub RGEVtFEkIFSQkLG
K62‑ub FEkIFSQkLGYLLFR
Y86‑p ARPLVEFyEEIKKyE
Y92‑p FyEEIKKyEKLETEE
K126‑ub ACSHPFSkSATEHVQ
K170‑ub QKFIESDkFTRFCQW
S247‑p RIMLSLVstGDCPFI
T248‑p IMLSLVstGDCPFIV
T263‑p CMSYAFHtPDKLSFI
K319‑ub FVVYRDLkPANILLD
K344‑ub GLACDFSkkKPHASV
K345‑ub LACDFSkkKPHASVG
Y356‑p ASVGTHGyMAPEVLQ
S416‑p MAVELPDsFSPELRS
K448‑ub GRGAQEVkESPFFRS
S487 ADAFDIGSFDEEDTK
S501‑p KGIKLLDsDQELyRN
Y506‑p LDsDQELyRNFPLTI
K628‑ub LLKIRGGkQFILQCD
K644‑ac DPELVQWkKELRDAY
S670‑p KMKNKPRsPVVELsk
S676‑p RsPVVELskVPLVQR
K677‑ub sPVVELskVPLVQRG
S685‑p VPLVQRGsANGL___
  rat

 
Y13 AVLADVSYLMAMEKS
S29‑p ATPAARAsKKILLPE
T54 LEDRGEVTFEKIFSQ
K57 RGEVTFEKIFSQKLG
K62 FEKIFSQKLGYLLFR
Y86 AKPLVEFYEEIEKYE
Y92 FYEEIEKYEKLETEE
K126 ACSHPFSKNATEHVQ
K170 HKFIESDKFTRFCQW
S247 RIMLSLVSTGDCPFI
T248 IMLSLVSTGDCPFIV
T263 CMSYAFHTPDKLSFI
K319 FVVYRDLKPANILLD
K344 GLACDFSKKKPHASV
K345 LACDFSKKKPHASVG
Y356 ASVGTHGYMAPEVLQ
S416 MAVELPDSFSPELRS
K448 GRGAQEIKESPFFRS
S487 ADAFDIGSFDEEDTK
S501 KGIKLLDSDQELYRN
Y506 LDSDQELYRNFPLTI
K628 LLKIRGGKQFVLQCD
K644 DPELVQWKKELRDAY
S670‑p KMKNKPRsPVVELSK
S676 RsPVVELSKVPLIQR
K677 sPVVELSKVPLIQRG
S685 VPLIQRGSANGL___
  cow

 
Y13‑p AVLADVSyLMAMEKS
S29 ATPAARASKKILLPE
T54 LEDRGEVTFEKIFSQ
K57 RGEVTFEKIFSQKLG
K62 FEKIFSQKLGYLLFR
Y86‑p AKPLVEFyEEIKKyE
Y92‑p FyEEIKKyEKLETEE
K126 ACSHPFSKSAIEHVQ
K170 QKFIESDKFTRFCQW
S247 RIMLSLVSTGDCPFI
T248 IMLSLVSTGDCPFIV
T263 CMSYAFHTPDKLSFI
K319 FVVYRDLKPANILLD
K344 GLACDFSKKKPHASV
K345 LACDFSKKKPHASVG
Y356 ASVGTHGYMAPEVLQ
S416 MAVELPDSFSPELRS
K448 GRGAQEVKESPFFRS
S487 ADAFDIGSFDEEDTK
S501 KGIKLLDSDQELYRN
Y506 LDSDQELYRNFPLTI
K628 LLKIRGGKQFVLQCD
K644 DPELVQWKKELRDAY
S670‑p KMKNKPRsPVVELSK
S676 RsPVVELSKVPLIQR
K677 sPVVELSKVPLIQRG
S685‑p VPLIQRGsANGL___
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