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FLASH GENE
Symbol CNR1 contributors: mct/npt - updated : 09-07-2017
HGNC name cannabinoid receptor 1 (brain)
HGNC id 2159
ASSOCIATED DISORDERS
corresponding disease(s)
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
tumoral     --low  
in clear cell renal cell carcinoma
constitutional     --over  
might cause abnormal decidualization and impair trophoblast invasion, thus being involved in the pathogenesis of preeclampsia
constitutional       loss of function
alleviates diabetes-mediated renal deterioration
constitutional       loss of function
combined deficiency of the CNR1 and CNR2 receptors protects against age-related bone loss by osteoclast inhibition
Susceptibility
  • to anorexia nervosa
  • to obesity related phenotypes
  • to hebephrenic schizophrenia
  • to sensitivity to the acute effects of cannabinoids on EP300 generation in healthy subjects
  • to diabetic nephropathy and diabetic retinopathy in patients with T2DM
  • Variant & Polymorphism other
  • variant increasing the risk of obesity related phenotypes
  • variant increasing the risk of hebephrenic schizophrenia
  • variations within CNR1 may differentially alter the sensitivity to the acute effects of cannabinoids on EP300 generation in healthy subjects
  • association of the G1359A polymorphism with diabetic nephropathy and diabetic retinopathy in patients with T2DM
  • Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    osteoarticularbone 
    treatment of osteoporosis and other bone diseases (antagonists of CNR1)
    digestive  
    use of cannabinoid CB(1) receptors in parietal cells as new therapeutic targets for the regulation of gastric acid production
    diabetetype 1 
    CNR1 inhibition may be beneficial in the treatment of diabetic retinopathy, a devastating complication of diabetes
    miscelleaneousurinarychronic kidney disease
    may be a new target for treating chronic kidney disease
    ANIMAL & CELL MODELS
  • mice lacking the Cnr1 gene, showed an accelerated age-dependent deficit in spatial learning accompanied by a loss of principal neurons in the hippocampus (