CLCNKB, Blocking Peptide

Chloride channel protein ClC-Kb; Chloride channel Kb; ClC-K2; CLCNKB

For Research Use Only. Not for use in diagnostic procedures.

Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.

Small volumes of CLCNKB blocking peptide vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms.

56,998 Da

chloride voltage-gated channel Kb

chloride channel protein ClC-Kb

Chloride channel protein ClC-Kb

Chloride channel Kb  [Similar Products]

CLCKB_HUMAN

The protein encoded by this gene is a member of the family of voltage-gated chloride channels. Chloride channels have several functions, including the regulation of cell volume, membrane potential stabilization, signal transduction and transepithelial transport. This gene is expressed predominantly in the kidney and may be important for renal salt reabsorption. Mutations in this gene are associated with autosomal recessive Bartter syndrome type 3 (BS3). Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2009]

CLCNKB: Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms. Defects in CLCNKB are the cause of Bartter syndrome type 3 (BS3); also known as classic Bartter syndrome. It is an autosomal recessive form of often severe intravascular volume depletion due to renal salt-wasting associated with low blood pressure, hypokalemic alkalosis, hypercalciuria, and normal serum magnesium levels. Defects in CLCNKB are a cause of Bartter syndrome type 4B (BS4B). A digenic, recessive disorder characterized by impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and varying degrees of hypercalciuria. Bartter syndrome type 4B is associated with sensorineural deafness. Belongs to the chloride channel (TC 2.A.49) family. CLCNKB subfamily.

Protein type: Membrane protein, multi-pass; Transporter, ion channel; Membrane protein, integral; Transporter

Chromosomal Location of Human Ortholog: 1p36

Cellular Component: integral to plasma membrane; plasma membrane

Molecular Function: voltage-gated chloride channel activity

Biological Process: excretion; transport

Disease: Bartter Syndrome, Type 3; Bartter Syndrome, Type 4b

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