GIRK2 (Kir3.2) Channel Overexpressed Membrane Fractions (#LX-102) are Xenopus oocyte membrane fractions overexpressing the Kir3.2 channel. GIRK2 (Kir3.2) Channel Overexpressed Membrane Fractions are your positive control for validating Alomone Labs Anti-GIRK2 (Kir3.2) Antibody (#APC-006).
Overexpressed Membrane Fractions are:
✓ Lyophilized powder
✓ Shipped at room temperature (no need for dry ice and extra shipping costs)
✓ User-friendly & time-saving. Just add water, sample buffer and load your gel
|Product Name||Cat #||Size|
|APC-006||1 x 0.2 ml|
|LX-102||1 x 0.1 ml|
Kir3.2 (or G-protein regulated inward-rectifier K+ channel, GIRK2) is a member of the family of inward rectifying K+ channels. The family includes 15 members that are structurally and functionally different from the voltage-dependent K+ channels.
The family’s topology consists of two transmembrane domains that flank a single and highly conserved pore region with intracellular N- and C-termini. As is the case for the voltage-dependent K+ channels, the functional unit for the Kir channels is composed of four subunits that can assemble as either homo- or heterotetramers.
Kir channels are characterized by a K+ efflux that is limited by depolarizing membrane potentials thus making them essential for controlling resting membrane potential and K+ homeostasis.
Kir3.2 is a member of the Kir3.x subfamily that includes four members (Kir3.1- Kir3.4). The Kir3 family is characterized by the fact that the channels can be activated by neurotransmitters and other factors acting via the activation of G-protein coupled receptors. Binding of the corresponding ligand to the G-protein receptor induces the dissociation of Gα-GTP from the Gbg dimer. The latter directly binds to Kir3 and activates the channel.2,3
Kir3.2 is mainly expressed in the brain, where it co-assembles with Kir3.1 (GIRK1) or Kir3.3 (GIRK3) and mediates the inhibitory effects of many neurotransmitters including opioid, adrenergic, muscarinic, dopaminergic and GABAergic neurotransmitters.2,3
Point mutations in the mouse Kir3.2 channel cause the weaver (wv) phenotype, a neurological abnormality characterized by the abnormal ‘weaving’ of the mice when they walk, hence the name weaver which is due to a substantial loss of cerebellar granule neurons. These mice also display mild local motor hyperactivity, presumably caused by the degeneration of dopaminergic neurons in the substantia nigra, spontaneous seizures and male sterility.1
A peptide toxin originating from the Apis mellifera bee venom, Tertiapin (#STT-250) was shown to be a potent blocker of Kir3.2 containing channels (7 nM for Kir3.2 alone and 5.4 nM for the Kir3.1/3.2 combination).4