Aliases for GNB5 Gene
External Ids for GNB5 Gene
Previous GeneCards Identifiers for GNB5 Gene
Heterotrimeric guanine nucleotide-binding proteins (G proteins), which integrate signals between receptors and effector proteins, are composed of an alpha, a beta, and a gamma subunit. These subunits are encoded by families of related genes. This gene encodes a beta subunit. Beta subunits are important regulators of alpha subunits, as well as of certain signal transduction receptors and effectors. Alternatively spliced transcript variants encoding different isoforms exist. [provided by RefSeq, Jul 2008]
GeneCards Summary for GNB5 Gene
GNB5 (G Protein Subunit Beta 5) is a Protein Coding gene. Diseases associated with GNB5 include Intellectual Developmental Disorder With Cardiac Arrhythmia and Language Delay And Adhd/Cognitive Impairment With Or Without Cardiac Arrhythmia. Among its related pathways are GABAergic synapse and p75 NTR receptor-mediated signalling. GO annotations related to this gene include GTPase activity and chaperone binding. An important paralog of this gene is GNB1.
UniProtKB/Swiss-Prot for GNB5 Gene
Enhances GTPase-activating protein (GAP) activity of regulator of G protein signaling (RGS) proteins, hence involved in the termination of the signaling initiated by the G protein coupled receptors (GPCRs) by accelerating the GTP hydrolysis on the G-alpha subunits, thereby promoting their inactivation (Probable). Increases RGS9 GTPase-activating protein (GAP) activity, hence contributes to the deactivation of G protein signaling initiated by D(2) dopamine receptors (PubMed:27677260). May play an important role in neuronal signaling, including in the parasympathetic, but not sympathetic, control of heart rate (By similarity).
Heterotrimeric G proteins are membrane bound GTPases that are linked to 7-TM receptors. Each G protein contains an alpha-, beta- and gamma-subunit and is bound to GDP in the 'off' state. Ligand binding causes a receptor conformational change, detaching the G protein and switching it 'on'.