KCNQ1 rabbit pAb
ENT-A9326
Description
| REF | ENT-A9326 |
|---|---|
| Category | Antibody Polyclonal |
| Description | KCNQ1 rabbit pAb |
| Source | Rabbit |
| Applications | WB;ELISA |
| Reactivity | Human;Rat;Mouse; |
| Reactivity | Human;Rat;Mouse; |
| Dilution | WB 1:500-2000 ELISA 1:5000-20000 |
| Immunogen | Synthesized peptide derived from human protein . at AA range: 350-430 |
| Storage Stability | -20°C/1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band KD | 74kD |
| Human Gene ID | 3784 |
| Human Swiss Prot Nº | P51787 |
| Subcellular Location | Cell membrane ; Multi-pass membrane protein . Cytoplasmic vesicle membrane . Early endosome . Membrane raft . Endoplasmic reticulum . Basolateral cell membrane . Colocalized with KCNE3 at the plasma membrane (PubMed:10646604). Upon 17beta-oestradiol treatment, colocalizes with RAB5A at early endosome (PubMed:23529131). Heterotetramer with KCNQ5 is highly retained at the endoplasmic reticulum and is localized outside of lipid raft microdomains (PubMed:24855057). During the early stages of epithelial cell polarization induced by the calcium switch it removed from plasma membrane to the endoplasmic reticulum where it retained and it is redistributed to the basolateral cell surface in a PI3K-dependent manner at a later stage (PubMed:21228319). . |
Other Name:
Background: This gene encodes a voltage-gated potassium channel required for repolarization phase of the cardiac action potential. This protein can form heteromultimers with two other potassium channel proteins, KCNE1 and KCNE3. Mutations in this gene are associated with hereditary long QT syndrome 1 (also known as Romano-Ward syndrome), Jervell and Lange-Nielsen syndrome, and familial atrial fibrillation. This gene exhibits tissue-specific imprinting, with preferential expression from the maternal allele in some tissues, and biallelic expression in others. This gene is located in a region of chromosome 11 amongst other imprinted genes that are associated with Beckwith-Wiedemann syndrome (BWS), and itself has been shown to be disrupted by chromosomal rearrangements in patients with BWS. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq,