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Key Documents

AV37678

Sigma-Aldrich

Anti-KCNAB2 (AB1) antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

Anti-Potassium voltage-gated channel, shaker-related subfamily, β member 2

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

100

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

40 kDa

Espèces réactives

guinea pig, dog, rat, bovine, horse, human, mouse, rabbit

Concentration

0.5 mg - 1 mg/mL

Technique(s)

immunohistochemistry: suitable
western blot: suitable

Numéro d'accès NCBI

NP_742128

Numéro d'accès UniProt

Q13303

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... KCNAB2(8514)

Description générale

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.

Immunogène

Synthetic peptide directed towards the middle region of human KCNAB2

Actions biochimiques/physiologiques

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.

Séquence

Synthetic peptide located within the following region: WGGKAETERGLSRKHIIEGLKASLERLQLEYVDVVFANRPDPNTPMEETV

Forme physique

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Charles Ashton et al.
Journal of neurosurgery, 1-7 (2020-02-29)
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
Vincent Portero et al.
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
H A Heilstedt et al.
Epilepsia, 42(9), 1103-1111 (2001-10-03)
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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