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Key Documents

Safety Information

AV35090

Sigma-Aldrich

Anti-KCNK3 antibody produced in rabbit

IgG fraction of antiserum

Synonym(s):

Anti-Potassium channel, subfamily K, member 3

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

43 kDa

species reactivity

dog, guinea pig, rat, sheep, human, bovine, mouse

concentration

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

NCBI accession no.

NP_002237

UniProt accession no.

O14649

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... KCNK3(3777)

General description

KCNK3 (TASK1) is a potassium channel protein that contains pore-forming domains. ML365 is known to selectively inhibit KCNK3. It is involved in the chemosensory regulation of breathing. KCNK3 variations have been linked to BP and aldosterone production.
Rabbit Anti-KCNK3 antibody recognizes human, mouse, rat, bovine, canine, and rabbit KCNK3.

Immunogen

Synthetic peptide directed towards the C terminal region of human KCNK3

Application

Rabbit Anti-KCNK3 antibody is suitable for western blot applications at a concentration of 1.25 μg/ml.

Biochem/physiol Actions

KCNK3 encodes one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. The gene product is an outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane. Although three transcripts are detected in northern blots, there is currently no sequence available to confirm transcript variants for this gene.

Sequence

Synthetic peptide located within the following region: TCVEQSHSSPGGGGRYSDTPSRRCLCSGAPRSAISSVSTGLHSLSTFRGL

Physical form

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

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Listings

Regulatory Listings are mainly provided for chemical products. Only limited information can be provided here for non-chemical products. No entry means none of the components are listed. It is the user’s obligation to ensure the safe and legal use of the product.

JAN Code

AV35090-100UG:
AV35090-100UL:

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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ML365: Development of Bis-Amides as Selective Inhibitors of the KCNK3/TASK1 Two Pore Potassium Channel.
Zou B, et al.
SourceProbe Reports from the NIH Molecular Libraries Program [Internet]. (2013)
Jeesun Jung et al.
The Journal of clinical endocrinology and metabolism, 97(11), E2160-E2167 (2012-08-16)
Two potassium (K) channel genes, Kcnk3 and Kcnk9, when deleted in mice, produced a model of hyperaldosteronism and hypertension. Our objective was to explore genetic variation [single-nucleotide polymorphisms (SNP)] in KCNK3 and KCNK9 in relation to blood pressure (BP) and
Stefan Trapp et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 28(35), 8844-8850 (2008-08-30)
Acid-sensitive K+ channels of the tandem P-domain K+-channel family (TASK-1 and TASK-3) have been implicated in peripheral and central respiratory chemosensitivity; however, because of the lack of decisive pharmacological agents, the final proof of the role of the TASK channel
Constanze Schmidt et al.
Circulation, 132(2), 82-92 (2015-05-09)
Antiarrhythmic management of atrial fibrillation (AF) remains a major clinical challenge. Mechanism-based approaches to AF therapy are sought to increase effectiveness and to provide individualized patient care. K(2P)3.1 (TASK-1 [tandem of P domains in a weak inward-rectifying K+ channel-related acid-sensitive

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