Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1) (cytoplasmic domain) Antikörper

Antigen: Potassium Inwardly-Rectifying Channel, Subfamily J, Member 1 (KCNJ1)

Synonyme: ROMK, ROMK1, KIR1.1, romk1, kir1.1, MGC86330, DKFZp469K0116, Kcnj, Romk2, Kir1.1, kcnj1, MGC68935, MGC63534, zgc:63534, wu:fl37c05

Epitope: cytoplasmic domain

Klonalität: Polyklonal

Wirt: Kaninchen

Applikation: Immunhistochemie (IHC), Western Blot (WB)

Produktnummer: ABIN350382

Produktbeschreibung

Weitere Bezeichnung: KCNJ1 (ROMK1, Kir1.1) (cytoplasmic domain)

Swiss-Prot: P48048

Immunogen: A synthetic peptide from the cytoplasmic domain of human KCNJ1 (ROMK1, Kir1.1) conjugated to an immunogenic carrier protein was used as the immunogen. The antigen is shares 92% identity with rat and mouse sequences.

Format: Lyophilized

Beschreibung: FUNCTION: In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium. Tissue specificity: In the kidney and pancreatic islets. Lower levels in skeletal muscle, pancreas, spleen, brain, heart and liver. Subcellular location: Membrane, Multi-pass membrane protein. Involvement in disease: Defects in KCNJ1 are the cause of Bartter syndrome type 2 (BS2) also termed hyperprostanglandin E syndrome 2. BS refers to a group of autosomal recessive disorders characterized by impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and varying degrees of hypercalciuria. BS2 is a life-threatening condition beginning in utero, with marked fetal polyuria that leads to polyhydramnios and premature delivery. Another hallmark of BS2 is a marked hypercalciuria and, as a secondary consequence, the development of nephrocalcinosis and osteopenia. Also known as: ATP-sensitive inward rectifier potassium channel 1, Potassium channel, inwardly rectifying subfamily J member 1, ATP-regulated potassium channel ROM-K, Kir1.1, ROMK1.

Spezifität: Appears to be specific for KCNJ1.

Anwendungen

Applikationshinweise: IHC, WB. A dilution of 1 : 300 to 1 : 2000 is recommended. The optimal dilution should be determined by the end user. Not yet tested in other applications.

Reinheit: whole serum

Lagerung: Maintain the lyophilised/reconstituted antibodies frozen at -20°C for long term storage and refrigerated at 2-8°C for a shorter term. When reconstituting, glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Publikationen

Publikationen: Krishnan, Desai, Ward et al.: "Isolation and chromosomal localization of a human ATP-regulated potassium channel." in: Human genetics, Vol. 96, Issue 2, pp. 155-60, 1995 (PubMed).

Shuck, Bock, Benjamin et al.: "Cloning and characterization of multiple forms of the human kidney ROM-K potassium channel." in: The Journal of biological chemistry, Vol. 269, Issue 39, pp. 24261-70, 1994 (PubMed).

Yano, Philipson, Kugler et al.: "Alternative splicing of human inwardly rectifying K+ channel ROMK1 mRNA." in: Molecular pharmacology, Vol. 45, Issue 5, pp. 854-60, 1994 (PubMed).

Simon, Karet, Rodriguez-Soriano et al.: "Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK." in: Nature genetics, Vol. 14, Issue 2, pp. 152-6, 1996 (PubMed).

Bock, Shuck, Benjamin et al.: "Nucleotide sequence analysis of the human KCNJ1 potassium channel locus." in: Gene, Vol. 188, Issue 1, pp. 9-16, 1997 (PubMed).

Sjoeblom, Jones, Wood et al.: "The consensus coding sequences of human breast and colorectal cancers." in: Science (New York, N.Y.), Vol. 314, Issue 5797, pp. 268-74, 2006 (PubMed).