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FLASH GENE
Symbol CNR1 contributors: mct/npt - updated : 09-07-2017
HGNC name cannabinoid receptor 1 (brain)
HGNC id 2159
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • seven transmembrane segments (7TM) receptor
  • C-terminus, having critical structures that are important for CB(1) activity and regulation
    • HOMOLOGY
    Homologene
    FAMILY
  • G protein coupled receptor superfamily
    • CATEGORY receptor membrane G
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,cytosolic,microsome
    basic FUNCTION
  • inhibiting adenylate cyclase located in and/or one cone pedicles and rod spherules
  • also inhibiting voltage-gated L-type calcium channel current in retinal bipolar cells
  • putatively involved for endogenous cannabinoid system in retinal physiology
  • play an unexpected role in dorsal horn pain-controlling circuits
  • participated in the regulation of lipid metabolism in human-derived immortalized hepatocytes by regulating the expression of key enzymes of lipid synthesis and transport
  • potential function in the early stages of corticogenesis
  • having a role in the regulation of bone mass
  • responsible for the psychotropic action of cannabinoids
  • could play an instrumental role in the development and function of the retina (
  • seems to be involved in the regulation of the EP300 wave as a marker of selective attention and working memory
  • its activity on hippocampal GABAergic neurons protects against age-dependent cognitive decline by reducing pyramidal cell degeneration and neuroinflammation
  • role of CNR1 in the regulation of Neural stem cells (NSCs) fate, suggesting that its activation may represent a pro-neuronal differentiation signal
  • endogenous CNR1 activation contributes to vascular SMC proliferation and neointima formation in response to arterial injury
  • play a critical role in LPS-induced febrile responses through inhibiting TLR4-mediated cytokine production
  • dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior
  • is not only associated with phenotypes such as cognitive performance, addiction and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions
  • has a major role in the activation of myofibroblasts
  • possibility of crosstalk between SST subtypes and CNR1 in regulation of physiological activities in the hippocampus
  • participate in the homeostatic responses regulating fluid balance and energy homeostasis during water deprivation
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
  • CNR1 signaling may thus play a role in physiological cardiorespiratory regulation and protect from some adverse cardiovascular consequences of a high-fat diet (HFD)
  • CNR1 signaling contributes to the hyperglycemia disturbance of PPARG2 signaling and increases inflammatory cytokine secretion and fibrotic matrix deposition in renal glomeruli
    • a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • tight control of CNR1 function by ADORA2A in glutamatergic terminals of the striatum
  • receptor binding &
    • 916;(9)-tetrahydrocannabinol, and implicated in several disease states, including drug addiction, anxiety, depression, obesity, and chronic pain
  • binding between a distal C-terminus fragment of cannabinoid receptor 1 CNR1) and arrestin-2 (ARRB2) (
  • ADORA2A and CNR1 may physically and functionally interact
  • CNR1 activation did not engage the key regulator of skin pigmentation, cyclic AMP, showing a major difference compared with the regulation of melanogenesis by alpha-melanocyte-stimulating hormone through MC1R
  • HINT1 protein cooperates with CNR1 to negatively regulate glutamate NMDA receptor activity
  • assembles with multiple members of the WASL complex and the RhoGTPase RAC1 and modulates their activity
    • cell & other
    REGULATION
    Other RARgamma regulates CNR1 expression and is thus involved in the control of hepatic fat metabolism by endocannabinoids
    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 (