GNAI3
GNAI3 (G protein subunit alpha i3, also known as 87U6) is an inhibitory alpha subunit of heterotrimeric G proteins. It transduces signals downstream of G protein-coupled receptors, inhibiting adenylate cyclase and lowering intracellular cAMP. Browse Assay Genie's current range of GNAI3 research reagents below, or read on for the biology behind the target.
Heterotrimeric G proteins act as transducers downstream of G protein-coupled receptors (GPCRs) in many signalling cascades. The GNAI3 alpha chain carries the guanine nucleotide binding site and alternates between an active, GTP-bound state and an inactive, GDP-bound state. Signalling by an activated GPCR promotes GDP release and GTP binding. The subunit has a low intrinsic GTPase activity that converts bound GTP to GDP and so terminates the signal; both GDP release and GTP hydrolysis are modulated by numerous regulatory proteins.
Signalling is mediated through effector proteins such as adenylate cyclase, which GNAI3 inhibits, leading to decreased intracellular cAMP levels. It also stimulates receptor-regulated K(+) channels. The active GTP-bound form activates the calcium-permeant TRPC5 ion channel, and it prevents the association of RGS14 with centrosomes, being required for the translocation of RGS14 from the cytoplasm to the plasma membrane. GNAI3 may also play a role in cell division. UniProt records the protein in the cytoplasm, at the cell membrane and at the centrosome.
The GNAI3 gene encodes an alpha subunit of the G-alpha family, within the G(i/o/t/z) subfamily, and HGNC places it in the group of G protein alpha subunits, group i, and among microRNA protein coding host genes. Its previous name was guanine nucleotide binding protein (G protein), alpha inhibiting activity polypeptide 3. A mutation resulting in a gly40-to-arg substitution is associated with auriculocondylar syndrome and affects downstream targets in the G protein-coupled endothelin receptor pathway. Mouse and rat orthologs are both named Gnai3.
GNAI3 couples activated G protein-coupled receptors to effectors, cycling between GTP-bound and GDP-bound states to start and terminate signalling.
By inhibiting adenylate cyclase, GNAI3 lowers intracellular cAMP levels, making it relevant to studies of second-messenger regulation.
GNAI3 stimulates receptor-regulated K(+) channels, and its GTP-bound form activates calcium-permeant TRPC5 channels.
A gly40-to-arg variant in GNAI3 is associated with auriculocondylar syndrome and alters signalling in the endothelin receptor pathway.
GNAI3 is a G protein alpha subunit that transduces signals from activated G protein-coupled receptors. In its GTP-bound state it inhibits adenylate cyclase, reducing cAMP, stimulates receptor-regulated K(+) channels and activates TRPC5 channels. Its intrinsic GTPase activity returns it to the inactive GDP-bound state.
The HGNC name is G protein subunit alpha i3, and UniProt lists it as guanine nucleotide-binding protein G(i) subunit alpha-3. The alias 87U6 is also used. An earlier name was guanine nucleotide binding protein (G protein), alpha inhibiting activity polypeptide 3.
A gly40-to-arg substitution in GNAI3 is associated with auriculocondylar syndrome and affects the G protein-coupled endothelin receptor pathway. Orthologs exist in mouse and rat, both called Gnai3; check the datasheet of any product for its validated reactivity.
Other inhibitory G protein alpha subunits and GPCR signalling targets with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P08754; product specifications from Assay Genie datasheets.