Overview
- Peptide (C)KLEESLREQAEKEGSALSVR, corresponding to amino acid residues 356-375 of rat Kir4.1 (Accession P49655). Intracellular, C-terminus.
- Rat and mouse brain membranes and human SH-SY5Y neuroblastoma cell lysate (1:800-1:1000).
Western blot analysis of rat brain membranes (lanes 1 and 4), mouse brain membranes (lanes 2 and 5) and human SH-SY5Y neuroblastoma cell lysates (lanes 3 and 6):1-3. Guinea pig Anti-Kir4.1 (KCNJ10) Antibody (#APC-035-GP), (1:800).
4-6. Guinea pig Anti-Kir4.1 (KCNJ10) Antibody, preincubated with Kir4.1/KCNJ10 Blocking Peptide (#BLP-PC035).- Following a broad screen of secondary antibodies, the following was used for this application: #106-035-006 (Jackson ImmunoResearch).
- Rat brain sections (1:300). Following a broad screen of secondary antibodies, the following was used for this application: #106-485-006 (Jackson ImmunoResearch).
- Human U-87 MG glioblastoma cell line.
Kir4.1 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 heteromers.
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.
Kir4.1 is a member of the Kir4 subfamily that includes one other member: Kir4.2. Kir4.1 can co-assemble with Kir4.2 but also with other Kir channels such as Kir2.1 and Kir5.1.
The Kir4 subfamily has been classified as weak rectifiers with intermediate conductance.
Kir4.1, encoded by KCNJ10, is mainly expressed in brain, specifically in glia cells, but also in retina, ear and kidney1,2.
It has been proposed that Kir4.1 has an essential role in glial K+ buffering, a process that re-uptakes the K+ released during neuronal activity into the intracellular interstitial space. Loss of Kir4.1 causes retinal defects and loss of endochoclear potential3.
Multiplex staining of Kir4.1 and α1-Syntrophin in rat fornixImmunohistochemical staining of immersion-fixed, free floating rat brain frozen sections using Guinea pig Anti-Kir4.1 (KCNJ10) Antibody (#APC-035-GP), (1:400) and Anti-α1-Syntrophin (SNTA1) Antibody (#APZ-021), (1:300). A. Kir4.1 staining (red) appears in blood vessel profiles (arrows) in the fornix. B. Syntrophin alpha 1 staining in the same section (green) appears in several elements including blood vessels (arrows). C. Merge of the two images reveals partial co-localization of Kir4.1 and syntrophin alpha 1 in hilar cells. Cell nuclei are stained with DAPI (blue).
