Anti-Kir3.2 (GIRK2)
- 貨號 Cat. No.
- APC-006
- 規格 Size
- 50 μl 0.2ml
Description
| Host: |
| Rabbit. |
| Epitope: |
GST fusion protein with sequence ELANRAEVPLSWSVS SKLNQHAELETEEEEKNPEELTERNG, corresponding to residues 374-414 of mouse Kir3.2 (Accession P48542) |
 |
| Putative epitope location: |
Intracellular, C-terminal part. |
| Homology: |
Rat, golden hamster, human - respectively, 40/41, 39/41, and 37/41 residues identical. |
Applications:
| Western Blotting: |
 | Western blotting of rat brain membranes: 1. Anti-Kir3.2 (GIRK2) (#APC-006) (1:200) 2. Anti-Kir3.2 (GIRK2), preincubated with the control antigen. |
| Immunohistochemistry: |
Rat brain sections |
| References: |
| 1. Hess, E.J. (1996) Neuron 16, 1073?076. |
| 2. Dascal, N. (1997) Cell Signal 9, 551?73. |
| 3. Mark, M.D. et al. (2000) Eur. J. Biochem. 267, 5830. |
| 4. Kubo, Y. et al. (2005) Pharmacol. Rev. 57, 509. |
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 familyî–¸ 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 Ga-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 theinhibitory effects of many neurotransmitters including opioid, adrenergic, muscarinic, dopaminergicand -aminobutyric acid (GABA).2,3
Point mutations in the mouse Kir3.2 channel cause the weaver (wv) phenotype, a neurologicalabnormality characterized bythe abnormal eaving?of the mice when they walk, hence thename weaver which is due to a substantial loss of cerebellargranule neurons. These mice also display mild local motorhyperactivity, presumably caused by the degeneration of dopaminergicneurons in the substantia nigra, spontaneous seizures and malesterility.1
A peptide toxin originating from the Apis mellifera bee venom, Tertiapin (#RTT-250) was shown to be a potent blocker of Kir3.2 containing channels (7nM for Kir3.2 alone and 5.4nM for the Kir3.1/3.2 combination).4