Dopamine receptor whose activity is mediated by G proteins which inhibit adenylyl cyclase. Defects in DRD2 are associated with dystonia type 11 (DYT11); also known as alcohol-responsive dystonia. DYT11 is a myoclonic dystonia. Dystonia is defined by the presence of sustained involuntary muscle contractions, often leading to abnormal postures. DYT11 is characterized by involuntary lightning jerks and dystonic movements and postures alleviated by alcohol. Inheritance is autosomal dominant. The age of onset, pattern of body involvement, presence of myoclonus and response to alcohol are all variable. Belongs to the G-protein coupled receptor 1 family. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Membrane protein, multi-pass; GPCR, family 1; Membrane protein, integral; Receptor, GPCR
Molecular Function: dopamine D2 receptor-like receptor activity; ionotropic glutamate receptor binding; identical protein binding; protein binding; potassium channel regulator activity; protein homodimerization activity; protein heterodimerization activity; dopamine binding; drug binding
Biological Process: response to nicotine; elevation of cytosolic calcium ion concentration during G-protein signaling, coupled to IP3 second messenger (phospholipase C activating); prepulse inhibition; positive regulation of dopamine uptake; response to toxin; positive regulation of receptor internalization; thermoregulation; positive regulation of multicellular organism growth; regulation of phosphoprotein phosphatase activity; adult walking behavior; dopamine metabolic process; dopamine receptor, adenylate cyclase inhibiting pathway; negative regulation of insulin secretion; protein localization; negative regulation of blood pressure; phosphatidylinositol metabolic process; response to drug; response to inactivity; positive regulation of neuroblast proliferation; response to light stimulus; cerebral cortex GABAergic interneuron migration; negative regulation of synaptic transmission, glutamatergic; regulation of sodium ion transport; arachidonic acid secretion; regulation of synaptic transmission, GABAergic; positive regulation of growth hormone secretion; G-protein coupled receptor internalization; reduction of cytosolic calcium ion concentration; activation of protein kinase activity; positive regulation of transcription from RNA polymerase II promoter; regulation of long-term neuronal synaptic plasticity; synaptic transmission, dopaminergic; peristalsis; branching morphogenesis of a nerve; negative regulation of circadian sleep/wake cycle, sleep; response to morphine; locomotory behavior; behavioral response to ethanol; orbitofrontal cortex development; negative regulation of cell proliferation; synaptogenesis; behavioral response to cocaine; visual learning; adenohypophysis development; nerve-nerve synaptic transmission; feeding behavior; response to axon injury; circadian regulation of gene expression; negative regulation of dopamine secretion; response to iron ion; negative regulation of cell migration; associative learning; positive regulation of cytokinesis; grooming behavior; negative regulation of protein secretion; negative regulation of protein kinase B signaling cascade; Wnt receptor signaling pathway; striatum development; regulation of heart rate; regulation of cAMP metabolic process; regulation of potassium ion transport; sensory perception of smell; response to amphetamine; negative regulation of adenylate cyclase activity; auditory behavior; regulation of dopamine uptake; response to cocaine; cellular calcium ion homeostasis; regulation of systemic arterial blood pressure by neurological process; negative regulation of dopamine receptor signaling pathway; pigmentation; axonogenesis; long-term memory; positive regulation of G-protein coupled receptor protein signaling pathway; release of sequestered calcium ion into cytosol; response to hypoxia; regulation of synapse structural plasticity; dopamine receptor, phospholipase C activating pathway
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.