Anti-CLC-K Antibody

CLC-K1, CLC-K2, CLC-Ka, CLC-Kb, Clcnka, Clcnkb, ClCk, Chloride channel K
    Cat #: ACL-004
    Alternative Name CLC-K1, CLC-K2, CLC-Ka, CLC-Kb, Clcnka, Clcnkb, ClCk, Chloride channel K
  • Lyophilized Powder
  • Antigen Incl.
  • Type: Polyclonal
    Host: Rabbit
    Reactivity: m, r
    May also work in: h*
    • Peptide (C)KKAISTLTNPPAPK, corresponding to amino acid residues 674-687 of the rat longer form CLC-K2L (Accession P51802). Intracellular, C-terminus.
    Accession (Uniprot) Number P51802
    Gene ID 79430
    Peptide confirmation Confirmed by amino acid analysis and mass spectrometry.
    Homology Mouse - identical; human - 13/14 amino acid residues identical.
    RRID AB_2039818.
    Purity Affinity purified on immobilized antigen.
    Form Lyophilized powder. Reconstituted antibody contains phosphate buffered saline (PBS), pH 7.4, 1% BSA, 5% sucrose, 0.025% NaN3.
    Isotype Rabbit IgG.
    Storage before reconstitution The antibody ships as a lyophilized powder at room temperature. Upon arrival, it should be stored at -20°C.
    Reconstitution 50 μl or 0.2 ml double distilled water (DDW), depending on the sample size.
    Antibody concentration after reconstitution 0.6 mg/ml.
    Storage after reconstitution The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods, small aliquots should be stored at -20°C. Avoid multiple freezing and thawing. Centrifuge all antibody preparations before use (10000 x g 5 min).
    Negative control antigen storage before reconstitution Lyophilized powder can be stored intact at room temperature for 2 weeks. For longer periods, it should be stored at -20°C.
    Negative control antigen reconstitution 100 µl double distilled water (DDW).
    Negative control antigen storage after reconstitution -20°C.
    Preadsorption Control 0.75 μg peptide per 1 μg antibody.
    Standard quality control of each lot Western blot analysis.
    Applications: if, ih, wb
    May also work in: ic*, ifc*, ip*
    Western blot
    • Anti-CLC-K Antibody
      Western blot analysis of rat kidney membranes:
      1. Anti-CLC-K Antibody (#ACL-004), (1:200).
      2. Anti-CLC-K Antibody, preincubated with the negative control antigen.
    • Rat kidney sections.
    1. Jentsch, T.J. et al. (2002) Physiol. Rev. 82, 503.
    2. Babini, E. and Pusch, M. (2004) Physiology 19, 293.
    3. Estevez, R. et al. (2001) Nature 414, 558.
    4. Simon, D.B. et al. (1997) Nat Genet 17, 171.
    Scientific background

    CLC-Ka and CLC-Kb are members of the voltage-dependent Cl- channel (CLC) family that includes nine known members in mammals. The human CLC-Ka and CLC-Kb (known as CLC-K1 and CLC-K2 in the rat) channels are closely related genes that share 94% sequence homology and identical genomic organization.

    CLC channels can be classified as plasma membrane channels and intracellular organelle channels. The first group includes the CLC-1CLC-2, CLC-Ka and CLC-Kb channels. The second group comprises the CLC-3, CLC-4, CLC-5, CLC-6 and CLC-7.

    CLC channels that function in the plasma membrane are involved in the stabilization of membrane potential and in transepithelial transport. The presumed function of the intracellular CLC channels is support of the acidification of the intraorganellar compartment. In this regard, recent reports indicate that CLC-4 and CLC-5 (and by inference CLC-3) can function as Cl-/H+ antiporters.1, 2

    The functional unit of the CLC channels is a dimer with each subunit forming a proper pore. Although the crystal structure of bacterial CLC channels was resolved,the topology of the CLC channels is complex and has not been fully elucidated. It is generally accepted that both the N- and C- terminus domains are intracellular while the number and configuration of the transmembrane domains vary greatly between different models. 1,2

    CLC-K channels require the presence of the auxiliary b subunit barttin, a 34 kD transmembrane protein, for transport to the plama membrane and regulation of channel permeation and gating.3

    CLC-K channels are expressed primarily in the kidney from the thin ascending limb to the collecting duct of the nephron, and in the stria vascularis and dark cells of the vestibular organ of the inner ear.

    The channels are important for renal salt reabsorption and water balance by enabling chloride exit across the basolateral membranes. The importance of the CLC-K channel in renal function is demonstrated by the fact that loss-of-function mutations in CLC-Kb lead to Bartter syndrome type III, an autosomal recessive disorder characterized by severe salt wasting, low blood pressure, hypokalemia and hypercalciuria.4

    Application key:

    CBE- Cell-based ELISA, FC- Flow cytometry, ICC- Immunocytochemistry, IE- Indirect ELISA, IF- Immunofluorescence, IFC- Indirect flow cytometry, IHC- Immunohistochemistry, IP- Immunoprecipitation, LCI- Live cell imaging, N- Neutralization, WB- Western blot

    Species reactivity key:

    H- Human, M- Mouse, R- Rat
    Image & Title:

    Anti-CLC-K Antibody
    Expression of CLC-K in mouse kidney.Immunohistochemical staining of mouse kidney sections using Anti-CLC-K Antibody (#ACL-004). CLC-K staining (red) appears in the thin ascending Loop of Henle. Claudin-4 staining is shown in red.Adapted from Fujita, H. et al. (2012) PLoS ONE 7, e52272. with permission of PLoS.

    Last update: 24/01/2020

    Anti-CLC-K Antibody (#ACL-004) is an antibody directed against an epitope of rat CLC-K2. The antibody can be used in western blot and immunohistochemistry applications. It has been designed to recognize CLC-K channel from rat, mouse, and human samples. The antibody recognizes both CLC-K1 and CLC-K2 isoforms.

    For research purposes only, not for human use



    Scientific Background


    Immunohistochemistry citations
    1. Mouse kidney sections (1:50).
      Akahoshi, N. et al. (2014) Am. J. Physiol. 306, F1462.
    2. Mouse kidney sections.
      Fujita, H. et al. (2012) PLoS ONE 7, 52272.
    More product citations
    1. Tagawa, H. et al. (2005) J. Biol. Chem. 280, 23876.
    2. Li, W.Y. et al. (2004) Am. J. Physiol. Renal Physiol. 286, F1063.
    3. Kiuchi-Saishin, Y. et al. (2002) J. Am. Soc. Nephrol. 13, 875.
    4. Klein, J. D. et al. (2002) Am. J. Physiol. Renal Physiol. 283, F517.
    5. Sage, C. L. et al. (2001) Hearing Res. 160, 1.
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