Drd1 encodes the mouse D(1A) dopamine receptor, a class A GPCR. UniProt summarizes the core function as "Dopamine receptor whose activity is mediated by G proteins which activate adenylyl cyclase" [UniProtKB:Q61616].
The strongest core GO terms are dopamine receptor activity coupled via Gs/Golf, dopamine binding, G-protein alpha-subunit binding, and adenylate cyclase-activating dopamine receptor signaling. The UniProt record also lists plasma membrane, ER membrane, ciliary membrane, dendrite, and dendritic spine localizations, so these cellular component terms are plausible, but most are contextual rather than the core activity [UniProtKB:Q61616].
Knockout and pharmacology literature strongly supports downstream phenotypes, but these should not be confused with molecular function. D1A knockout mice lack striatal D1A receptor binding and show altered striatal function, including reduced rearing behavior PMID:7809078. D1 receptor mutant mice also fail to show normal cocaine-induced locomotor stimulation and dopamine-mediated nucleus accumbens electrophysiological responses PMID:8001143.
Synaptic plasticity annotations are biologically relevant but downstream. D1-deficient mice show defective late-phase hippocampal LTP PMID:9427321, and striatal studies distinguish D1 and D5 receptor roles in motor activity and plasticity PMID:13679419.
PLC/calcium annotations should be treated as specialized non-core signaling. The D1-D2 dopamine receptor heteromer paper reports a complex that activates Gq/11 and intracellular calcium release PMID:17194762. This supports retaining phospholipase C-activating dopamine receptor signaling as non-core, not as the general Drd1 pathway.
Trafficking and ciliary annotations are supported but contextual. SLC35D3 interacts with D1R and affects ER exit and plasma membrane delivery PMID:24550737. VPS35 regulates DRD1 recycling and downstream CREB/ERK phosphorylation PMID:27460146. TULP3/TUB work supports ciliary trafficking of D1R as one specialized localization context PMID:28154160.
Generic protein binding, signaling receptor binding, heterocyclic compound binding, signal transduction, vasodilation, and computational behavioral predictions are weak as direct Drd1 functional annotations. They were marked over-annotated where the more specific receptor, ligand-binding, G-protein coupling, or pathway terms already represent the underlying biology.