KCNQ1 Polyclonal Antibody (E-AB-60659)
For research use only.
| Verified Samples |
Verified Samples in WB: HT29, SW620, Mouse kidney, BT-474 |
| Dilution | WB 1:500-1:2000 |
| Isotype | IgG |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Applications | WB |
| Clonality | Polyclonal |
| Immunogen | Recombinant fusion protein of human KCNQ1 (NP_861463.1). |
| Abbre | KCNQ1 |
| Synonyms | ATFB1, ATFB3, JLNS1, KCNA8, KCNA9, KCNQ1, KVLQT1, Kv1.9, Kv7.1, LQT, LQT1, RWS, SQT2, WRS |
| Swissprot | |
| Calculated MW | 61 kDa/74 kDa |
| Observed MW |
70 kDa
The actual band is not consistent with the expectation.
Western blotting is a method for detecting a certain protein in a complex sample based on the specific binding of antigen and antibody. Different proteins can be divided into bands based on different mobility rates. The mobility is affected by many factors, which may cause the observed band size to be inconsistent with the expected size. The common factors include: 1. Post-translational modifications: For example, modifications such as glycosylation, phosphorylation, methylation, and acetylation will increase the molecular weight of the protein. 2. Splicing variants: Different expression patterns of various mRNA splicing bodies may produce proteins of different sizes. 3. Post-translational cleavage: Many proteins are first synthesized into precursor proteins and then cleaved to form active forms, such as COL1A1. 4. Relative charge: the composition of amino acids (the proportion of charged amino acids and uncharged amino acids). 5. Formation of multimers: For example, in protein dimer, strong interactions between proteins can cause the bands to be larger. However, the use of reducing conditions can usually avoid the formation of multimers. If a protein in a sample has different modified forms at the same time, multiple bands may be detected on the membrane. |
| Cellular Localization | Cell membrane. 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). |
| Concentration | 1 mg/mL |
| Buffer | Phosphate buffered solution, pH 7.4, containing 0.05% stabilizer and 50% glycerol. |
| Purification Method | Affinity purification |
| Research Areas | Cancer, Cardiovascular, Metabolism, Neuroscience, Signal Transduction |
| Conjugation | Unconjugated |
| Storage | Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles. |
| Shipping | The product is shipped with ice pack,upon receipt,store it immediately at the temperature recommended. |
| 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. |
Other Clones
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Unconjugated
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