|Calculated MW||44963 Da|
|Homology||Mouse - identical; human - 45/50 amino acid residues identical.|
|Other Names||ATP-sensitive inward rectifier potassium channel 1, ATP-regulated potassium channel ROM-K, Inward rectifier K(+) channel Kir11, KAB-1, Potassium channel, inwardly rectifying subfamily J member 1, Kcnj1, Romk1|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||GST fusion protein with sequence HNFGKTVEVETPHCAMCLYNEKDARARMKRGYDNPNFVLSEVDET DDTQM, corresponding to amino acids 342-391 of rat ROMK1 (Accession P35560), (MW: 33 kDa).ֲ Intracellular, C-terminus.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|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 PBS.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||3 µg fusion protein per 1 µg antibody.|
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Provided below are standard protocols that you may find useful for product applications.
Kir1.1 (ROMK1) was the first member of the family of inward rectifying K+ channels to be cloned.1 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 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.3 As its original name indicates (ROMK1 stands for Renal Outer Medullary K+ channel) Kir1.1 is strongly expressed in the kidney in the apical membrane of several kidney segments such as the thick ascending loop of Henle (TAL) and the cortical collecting duct (CCD). In addition, the channel is also expressed in the brain mainly in the cortex and hippocampus.3 Kir1.1 plays a key role in K+ recycling in the loop of Henle. Indeed, loss of function mutations in the Kir1.1 gene cause Bartter’s syndrome type II, a recessive autosomal disease characterized by the impairment of K+ efflux and the subsequent inability of the NKCC2 transporter to continue NaCl uptake. This leads to a high salt concentration in the urine that induces osmotic diuresis and low plasma volume.2 Pharmacologically, the Kir1.1 channel can be inhibited by several general K+ channel blockers such as Tertiapin (#STT-250), however the scorpion toxin Lq2 (#RTL-550) specifically and potently inhibits Kir1.1 channels.4
References 1. Ho, K. et al. (1993) Nature 362, 31. 2. Simon, D.B. et al. (1996) Nat. Genet. 14, 152. 3. Wang, W-H. (2006) Am. J. Physiol. Renal Physiol. 290, F14. 4. Lu, Z. and McKinnon, R. (1997) Biochemistry 36, 6936.
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