We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality Kir3.2 (GIRK2) antibody.

48652 Da

Rabbit

Human, Mouse, Rat

GST fusion protein with sequence ELANRAEVPLSWSVS SKLNQHAELETEEEEKNPEELTERNG, corresponding to residues 374-414 of mouse Kir3.2? (Accession P48542), (MW: 31 kDa.).?Intracellular, C-terminal part.

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 subunit that can assembly 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, were it co-assembles with Kir3.1 or Kir3.3 and mediates the inhibitory effects of many neurotransmitters including opioid, adrenergic, muscarinic, dopaminergic and γ-aminobutyric acid (GABA).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

Affinity purified antibody, Liquid

Store at +4°C short term. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.

WB, IHC, IP, ICC

WB~~1:200-1:2000

G protein-activated inward rectifier potassium channel 2, GIRK-2, Inward rectifier K(+) channel Kir32, Potassium channel, inwardly rectifying subfamily J member 6, Kcnj6, Girk2, Kcnj7, W

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