Potassium voltage-gated channel subfamily A regulatory beta subunit 2 (KCNAB2), an ion channel gene, codes for a voltage?gated K+ channel β?subunit protein, Kvβ2. This gene is located on human chromosome 1p36. Kvβ2 is expressed ubiquitously in the human heart. It belongs to the aldo?keto reductase superfamily. This member is one of the beta subunits, which are auxiliary proteins associating with functional Kv-α subunits.
Immunogen
Synthetic peptide directed towards the middle region of human KCNAB2
Biochem/physiol Actions
Potassium voltage-gated channel subfamily A regulatory β subunit 2 (KCNAB2) gene is involved in neuroendocrine conditions KCNAB2 serves as a candidate gene for epilepsy. A cardiac arrhythmia disorder, called Brugada syndrome occurs due to the gain-of-function mutation in KCNAB2 gene. Voltage-gated potassium (Kv) channels play a key role in modulating the contraction of smooth muscle, secretion of insulin, the release of neurotransmitters, and excitability of the neuron. It also participates in heart rate, epithelial electrolyte transport, and cell volume.
Sequence
Synthetic peptide located within the following region: WGGKAETERGLSRKHIIEGLKASLERLQLEYVDVVFANRPDPNTPMEETV
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
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Prior profiling of the human pituitary adenoma (PA) DNA methylome showed the potassium channel subunit-encoding gene KCNAB2 to be highly differentially methylated between nonfunctional PAs (NFPAs) and growth hormone (GH)-secreting PAs, with greater KCNAB2 methylation detected in secretory PAs. KCNAB2
Journal of the American Heart Association, 5(6) (2016-06-12)
The Brugada syndrome is an inherited cardiac arrhythmia associated with high risk of sudden death. Although 20% of patients with Brugada syndrome carry mutations in SCN5A, the molecular mechanisms underlying this condition are still largely unknown. We combined whole-exome sequencing
Clinical features associated with chromosome 1p36 deletion include characteristic craniofacial abnormalities, mental retardation, and epilepsy. The presence and severity of specific phenotypic features are likely to be correlated with loss of a distinct complement of genes in each patient. We
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