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Gene Ontology Classifications
Symbol
Name
ID
Vkorc1
vitamin K epoxide reductase complex, subunit 1
MGI:106442

Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Vkorc1. (This text reflects annotations as of Thursday, July 24, 2014.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 9, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq


Vitamin K is essential for blood clotting but must be enzymatically activated. This enzymatically activated form of vitamin K is a reduced form required for the carboxylation of glutamic acid residues in some blood-clotting proteins. The product of this gene encodes the enzyme that is responsible for reducing vitamin K 2,3-epoxide to the enzymatically activated form. Fatal bleeding can be caused by vitamin K deficiency and by the vitamin K antagonist warfarin, and it is the product of this gene that is sensitive to warfarin. In humans, mutations in this gene can be associated with deficiencies in vitamin-K-dependent clotting factors and, in humans and rats, with warfarin resistance. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text for additional MGI annotations
References
  1. Pelz HJ et al. (2005) The genetic basis of resistance to anticoagulants in rodents. Genetics, 170:1839-47. (PubMed:15879509)
  2. Spohn G et al. (2009) VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. Thromb Haemost, 101:1044-50. (PubMed:19492146)



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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IMP Inferred from mutant phenotype
  IPI Inferred from physical interaction
  ISS Inferred from sequence or structural similarity
  ISO Inferred from sequence orthology
  ISA Inferred from sequence alignment
  ISM Inferred from sequence model
  NAS Non-traceable author statement
  ND No biological data available
  RCA Reviewed computational analysis
  TAS Traceable author statement


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
12/09/2014
MGI 5.20
The Jackson Laboratory