Overview

  • Product name

  • Description

    Rabbit polyclonal to CLCNKB
  • Host species

    Rabbit
  • Tested applications

    Suitable for: IHC-P, WB, ICC/IFmore details
  • Species reactivity

    Reacts with: Rat, Human
  • Immunogen

    Recombinant fragment corresponding to Human CLCNKB aa 538-687.
    Sequence:

    RNIGSHRVRVEHFMNHSITTLAKDMPLEEVVKVVTSTDVAKYPLVESTES QILVGIVRRAQLVQALKAEPPSWAPGHQQCLQDILAAGCPTEPVTLKLSP ETSLHEAHNLFELLNLHSLFVTSRGRAVGCVSWVEMKKAISNLTNPPAPK


    Database link: P51801

  • Positive control

    • WB: HeLa whole cell lysate; Rat kidney tissue lysate. IHC-P: Human breast cancer tissue. ICC/IF: HepG2 cells.

Properties

Applications

Our Abpromise guarantee covers the use of ab236733 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P 1/200 - 1/500.
WB 1/500 - 1/5000. Predicted molecular weight: 75 kDa.
ICC/IF 1/50 - 1/200.

Target

  • Function

    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.
  • Tissue specificity

    Expressed predominantly in the kidney.
  • Involvement in disease

    Defects in CLCNKB are the cause of Bartter syndrome type 3 (BS3) [MIM:607364]; 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) [MIM:613090]. 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.
  • Sequence similarities

    Belongs to the chloride channel (TC 2.A.49) family. CLCNKB subfamily.
    Contains 2 CBS domains.
  • Cellular localization

    Cell membrane.
  • Information by UniProt
  • Database links

  • Alternative names

    • Bartter syndrome type 3 antibody
    • Chloride channel Kb antibody
    • Chloride channel kidney B antibody
    • Chloride channel protein ClC-Kb antibody
    • Chloride channel voltage sensitive Kb antibody
    • ClC K2 antibody
    • ClC-K2 antibody
    • ClCK2 antibody
    • CLCKB antibody
    • CLCKB_HUMAN antibody
    • CLCNKB antibody
    • hClC Kb antibody
    • hClCKb antibody
    • MGC24087 antibody
    • OTTHUMP00000011120 antibody
    • OTTHUMP00000011121 antibody
    • RP11 5P18.8 antibody
    see all

Images

  • Paraffin-embedded human breast cancer tissue stained for CLCNKB using ab236733 at 1/300 dilution in immunohistochemical analysis.

    After dewaxing and hydration, antigen retrieval was mediated by high pressure in a citrate buffer (pH 6.0). Section was blocked with 10% normal goat serum 30 minutes at RT. Then primary antibody (1% BSA) was incubated at 4°C overnight. The primary is detected by a biotinylated secondary antibody and visualized using an HRP conjugated SP system.

  • All lanes : Anti-CLCNKB antibody (ab236733) at 1/500 dilution

    Lane 1 : HeLa (human epithelial cell line from cervix adenocarcinoma) whole cell lysate
    Lane 2 : Rat kidney tissue lysate

    Secondary
    All lanes : Goat polyclonal to rabbit IgG at 1/50000 dilution

    Predicted band size: 75 kDa

  • HepG2 (human liver hepatocellular carcinoma cell line) cells labeling CLCNKB (Green) using ab236733 at 1/100 dilution in ICC/IF, followed by Alexa Fluor® 488-congugated Goat Anti-Rabbit IgG (H+L). Counterstained with DAPI.

    The cells were fixed in 4% formaldehyde, permeabilized using 0.2% Triton X-100 and blocked in 10% normal Goat Serum.

References

ab236733 has not yet been referenced specifically in any publications.

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