|Application ||WB, IP|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||42480 Da|
|Homology||Human, mouse - identical.|
|Other Names||ATP-sensitive inward rectifier potassium channel 10, ATP-sensitive inward rectifier potassium channel KAB-2, BIR10, Brain-specific inwardly rectifying K(+) channel 1, BIRK1, Inward rectifier K(+) channel Kir41, Potassium channel, inwardly rectifying subfamily J member 10, Kcnj10, Kab-2|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)KLEE SLREQ AEKEG SALSV R, corresponding to amiono acid residues 356-375 of rat Kir4.1 (Accession P49655). Intracellular, C-terminus.|
|Peptide Confirmation||Confirmed by mass-spectrography and amino acid analysis.|
|Application Details||Western blot analysis (WB): - Mouse cerebellum lysate (1:500) (see Winkler, U. et al. (2013) in Product Citations). - Rat brain lysate (1:500) (see Harada, Y. et al. (2013) in Product Citations). Immunoprecipitation (IP): - Rat renal cortex lysate (Cha, S.K. et al. (2011) in Product Citations). Immunohistochemistry (IH): - Mouse ear sections (1:400) (see Stevens, S.M. et al. (2014) in Product Citations). - Mouse cochlea (1:300) (see Girotto, G. et al. (2013) in Product Citations). - Rat formalin-fixed paraffin-embedded brain sections (1:50-1:100) (see Harada, Y. et al. in Product Citations). - Mouse stria vascularis (see Buniello, A. et al. (2013) in Product Citations). - Mouse hippocampus (1:200) (see Hsu, M.S. et al. (2011) in Product Citations). - Human brain tissue (see Saadoun, S. et. al. (2003) in Product Citations). Immunocytochemistry (IC): - Mouse outer hair cells (OHCs) (see Ruttinger, L. et al. (2004) in product Citations).|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.4 mg/ml.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
|Formulation||Lyophilized powder. Reconstituted antibody contains phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.05% NaN3.|
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Provided below are standard protocols that you may find useful for product applications.
Kir4.1 is a member of the inward rectifying K+ channel family. 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 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 is mainly expressed in brain, specifically in glia cells, but also in retina, ear and kidney.1,2 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 potential.3
References 1. Takumi, T. et al. (1995) J. Biol. Chem. 270,16339. 2. Higashi, K. et al. (2001) Am. J. Physiol. 281, C922. 3. Butt, A.M. and Kalsi, A. (2006) J. Cell Mol. Med. 10, 33.
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