Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation by the MGI curatorial staff, curated orthology
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
Paradoxical locomotor behavior of dopamine D1 receptor transgenic mice.
Spatial learning deficit in dopamine D(1) receptor knockout mice.
Behavioral responses to cocaine and amphetamine administration in mice lacking the dopamine D1 receptor.
Modification of dopamine D(1) receptor knockout phenotype in mice lacking both dopamine D(1) and D(3) receptors.
Dopamine D2 long receptor-deficient mice display alterations in striatum-dependent functions.
Distinct functions of the two isoforms of dopamine D2 receptors.
Prepulse inhibition deficits and perseverative motor patterns in dopamine transporter knock-out mice: differential effects of D1 and D2 receptor antagonists.
Prolonged fear responses in mice lacking dopamine D1 receptor.
Blunted brain metabolic response to ketamine in mice lacking D(1A) dopamine receptors.
Galpha(olf) levels are regulated by receptor usage and control dopamine and adenosine action in the striatum.
The role of dopamine receptors in regulating the size of axonal arbors.
Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice.
Alpha1b-adrenergic receptors control locomotor and rewarding effects of psychostimulants and opiates.
-
D1 agonist response was used to rule out basal dopaminergic compensation in alpha1b-adrenergic receptor knockout mice, not to directly test Drd1 adenylyl-cyclase signaling.
"Because catecholamine tissue levels, autoradiography of D1 and D2 dopaminergic receptors, and of dopamine reuptake sites and locomotor response to a D1 agonist showed that basal dopaminergic transmission was similar in knock-out and wild-type mice"
Phenotypic resolution of spontaneous and D1-like agonist-induced orofacial movement topographies in congenic dopamine D1A receptor 'knockout' mice.
Mice lacking dopamine D2 and D3 receptors have spatial working memory deficits.
Impaired D2 dopamine receptor function in mice lacking type 5 adenylyl cyclase.
-
Type 5 adenylyl cyclase loss eliminates most striatal D1 agonist-stimulated adenylyl cyclase activity, supporting D1 receptor coupling to AC5/cAMP signaling.
"The genetic ablation of the AC5 gene eliminated >80% of forskolin-induced AC activity and 85-90% of AC activity stimulated by either D1 or A2A receptor agonists in striatum."
-
AC5 is presented as a striatal signaling integrator for D1, D2, and A2A receptors.
"Together, these results suggest that AC5 is the principal AC integrating signals from multiple receptors including D1, D2, and A2A in striatum"
The dopamine D1 receptor is a critical mediator for cocaine-induced gene expression.
Loss of G protein gamma 7 alters behavior and reduces striatal alpha(olf) level and cAMP production.
Attenuation of sucrose reinforcement in dopamine D1 receptor deficient mice.
Essential conservation of D1 mutant phenotype at the level of individual topographies of behaviour in mice lacking both D1 and D3 dopamine receptors.
Motor dysfunction in type 5 adenylyl cyclase-null mice.
-
D1 dopaminergic agonist-stimulated adenylyl cyclase activity is attenuated in AC5-null striatum, supporting Drd1/AC5/cAMP pathway coupling.
"D1 dopaminergic agonist-stimulated adenylyl cyclase activity was attenuated, and this was accompanied by a decrease in the expression of the D1 dopaminergic receptor and G(s)alpha."
-
D1 stimulation partially compensates through remnant adenylyl cyclase isoforms in AC5-null mice.
"Selective D1 or D2 dopaminergic stimulation improved some of these disorders in this mouse model, suggesting the partial compensation of each dopaminergic receptor signal through the stimulation of remnant adenylyl cyclase isoforms."
Receptor subtypes involved in the presynaptic and postsynaptic actions of dopamine on striatal interneurons.
Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons.
Distinct roles of D1 and D5 dopamine receptors in motor activity and striatal synaptic plasticity.
G-protein-coupled receptor-mediated activation of rap GTPases: characterization of a novel Galphai regulated pathway.
Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors.
Enhancement of dopamine-induced signaling responses in the forebrain of mice lacking dopamine D3 receptor.
Simultaneous absence of dopamine D1 and D2 receptor-mediated signaling is lethal in mice.
Dopamine D1 receptors involved in locomotor activity and accumbens neural responses to prediction of reward associated with place.
Mice lacking dopamine D1 receptors express normal lithium chloride-induced conditioned taste aversion for salt but not sucrose.
Expression of mutant NMDA receptors in dopamine D1 receptor-containing cells prevents cocaine sensitization and decreases cocaine preference.
Binding of internalized receptors to the PDZ domain of GIPC/synectin recruits myosin VI to endocytic vesicles.
Low affinity binding of the classical D1 antagonist SCH23390 in rodent brain: potential interaction with A2A and D2-like receptors.
D1-D2 dopamine receptor heterooligomers with unique pharmacology are coupled to rapid activation of Gq/11 in the striatum.
Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior.
Dopamine receptor activation modulates GABA neuron migration from the basal forebrain to the cerebral cortex.
Lack of self-administration of cocaine in dopamine D1 receptor knock-out mice.
Hyperthermic and lethal effects of methamphetamine: roles of dopamine D1 and D2 receptors.
A phosphatase cascade by which rewarding stimuli control nucleosomal response.
Decrease of D2 receptor binding but increase in D2-stimulated G-protein activation, dopamine transporter binding and behavioural sensitization in brains of mice treated with a chronic escalating dose 'binge' cocaine administration paradigm.
Balanced NMDA receptor activity in dopamine D1 receptor (D1R)- and D2R-expressing medium spiny neurons is required for amphetamine sensitization.
Regulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core.
Prostaglandin E receptor EP1 forms a complex with dopamine D1 receptor and directs D1-induced cAMP production to adenylyl cyclase 7 through mobilizing G(βγ) subunits in human embryonic kidney 293T cells.
Mutation of SLC35D3 causes metabolic syndrome by impairing dopamine signaling in striatal D1 neurons.
A critical time window for dopamine actions on the structural plasticity of dendritic spines.
Drebrin depletion alters neurotransmitter receptor levels in protein complexes, dendritic spine morphogenesis and memory-related synaptic plasticity in the mouse hippocampus.
Identification of G Protein-Coupled Receptors (GPCRs) in Primary Cilia and Their Possible Involvement in Body Weight Control.
Dopamine synapse is a neuroligin-2-mediated contact between dopaminergic presynaptic and GABAergic postsynaptic structures.
VPS35 regulates cell surface recycling and signaling of dopamine receptor D1.
Tubby family proteins are adapters for ciliary trafficking of integral membrane proteins.
Role of D1/D2 dopamine and N-methyl-D-aspartate (NMDA) receptors in morphine tolerance and dependence in mice.
Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors.
Altered striatal function in a mutant mouse lacking D1A dopamine receptors.
Dopamine D1 receptor mutant mice are deficient in striatal expression of dynorphin and in dopamine-mediated behavioral responses.
Elimination of cocaine-induced hyperactivity and dopamine-mediated neurophysiological effects in dopamine D1 receptor mutant mice.
Lesions of mouse striatum induced by 6-hydroxydopamine differentially alter the density, rate of synthesis, and level of gene expression of D1 and D2 dopamine receptors.
Differences among mouse strains in the regulation by mu, delta 1 and delta 2 opioid receptors of striatal adenylyl cyclases activated by dopamine D1 or adenosine A2a receptors.
Modulatory actions of dopamine on NMDA receptor-mediated responses are reduced in D1A-deficient mutant mice.
D1-like dopaminergic activation of phosphoinositide hydrolysis is independent of D1A dopamine receptors: evidence from D1A knockout mice.
Effects of repeated amphetamine treatment on the locomotor activity of the dopamine D1A-deficient mouse.
Dopamine D3 receptor mutant mice exhibit increased behavioral sensitivity to concurrent stimulation of D1 and D2 receptors.
D1 receptors mediate dopamine action in the fetal suprachiasmatic nuclei: studies of mice with targeted deletion of the D1 dopamine receptor gene.
Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation.
Behavioural assessment of mice lacking D1A dopamine receptors.
Action sequencing is impaired in D1A-deficient mutant mice.
Dopamine-stimulated sexual behavior is testosterone dependent in mice.
The expression of neuropeptide-induced excessive grooming behavior in dopamine D1 and D2 receptor-deficient mice.
UniProt record for mouse Drd1 (Q61616)
-
Drd1 is a dopamine receptor mediated by G proteins that activate adenylyl cyclase.
-
UniProt places Drd1 at cell membrane, ER membrane, ciliary membrane, dendrite, and dendritic spine contexts.
Falcon deep research summary for mouse Drd1
-
Falcon synthesis supports Drd1 as a D1-like class A GPCR whose core output is Gs/Golf-mediated adenylyl cyclase activation and cAMP/PKA signaling.
-
Falcon synthesis treats ciliary, endosomal, dendritic-spine, and receptor-complex signaling as important but context-specific Drd1 biology.