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Protein Page:
GPVI (human)

Overview
GPVI Collagen receptor involved in collagen-induced platelet adhesion and activation. Plays a key role in platelet procoagulant activity and subsequent thrombin and fibrin formation. This procoagulant function may contribute to arterial and venous thrombus formation. The signaling pathway involves the FcR gamma- chain, the Src kinases (likely Fyn/Lyn), the adapter protein LAT and leads to the activation of phospholipase C gamma2. Defects in GP6 are the cause of bleeding disorder platelet-type 11 (BDPLT11). BDPLT11 is a mild to moderate bleeding disorder caused by defective platelet activation and aggregation in response to collagen. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Membrane protein, integral
Chromosomal Location of Human Ortholog: 19q13.4
Cellular Component: cell surface; integral to plasma membrane; plasma membrane
Molecular Function: collagen binding; protein binding; receptor activity; transmembrane receptor activity
Biological Process: blood coagulation; enzyme linked receptor protein signaling pathway; leukocyte migration; platelet activation
Disease: Bleeding Disorder, Platelet-type, 11
Reference #:  Q9HCN6 (UniProtKB)
Alt. Names/Synonyms: Glycoprotein 6; glycoprotein VI (platelet); GP6; GPIV; GPVI; MGC138168; platelet collagen receptor; Platelet glycoprotein VI
Gene Symbols: GP6
Molecular weight: 36,866 Da
Basal Isoelectric point: 9.35  Predict pI for various phosphorylation states
Select Structure to View Below

GPVI

Protein Structure Not Found.


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Modification Sites and Domains  

Modification Sites in Parent Protein, Orthologs, and Isoforms  
 

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.


       human

 
0 1 Y67‑p EKLSSSRyQDQAVLF
  mouse

 
Y68 EKLKPEKYEDQDFLF
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