C1116
Anti-Chloride Channel CLC-5 (Clcn5) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-CLC5, Anti-CLCK2, Anti-ClC-5, Anti-DENT1, Anti-DENTS, Anti-NPHL1, Anti-NPHL2, Anti-XLRH, Anti-XRN
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About This Item
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
human, mouse, rat
technique(s)
western blot: 1:200 using rat kidney membranes
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CLCN5(1184)
mouse ... Clcn5(12728)
rat ... Clcn5(25749)
Immunogen
peptide corresponding to amino acid residues 401-415 of rat CLC5. Mouse sequence is identical; human sequence is 14/15 residues identical.
Application
Anti-Chloride Channel CLC-5 (Clcn5) antibody produced in rabbit is suitable for western blotting at a dilution of 1:200 using rat kidney membranes.
Biochem/physiol Actions
H(+)/Cl(-) exchange transporter 5 is a protein encoded by the CLCN5 gene in humans. It encodes a member of the CLC gene family of chloride ion channels and ion transporters. CLCN5 is highly expressed in endosomes of proximal tubule cells and is essential for endocytosis. Mutations in CLCN5 causes Dent′s disease leading to renal failure. It is also involved in low-molecular-weight proteinuria, hypercalciuria, nephrolithiasis and renal failure. Majority of these disease-causing mutations in ClC-5 are misprocessed and retained in the ER (endoplasmic reticulum) and may alter intramolecular interactions within the full-length ClC-5 protein. CLC-5 plays a crucial role in the process of endocytosis in the proximal tubule of the kidney and mutations that alter protein function are the cause of Dent′s disease. It may act as an electrically shunting Cl- channel in early endosomes, facilitating intraluminal acidification.
Physical form
Lyophilized from phosphate buffered saline containing, pH 7.4, 1% BSA and 0.05% sodium azide
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
11 - Combustible Solids
WGK
WGK 2
Certificates of Analysis (COA)
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Silvia De Stefano et al.
The Journal of physiology, 591(23), 5879-5893 (2013-10-09)
ClC-5 is a 2Cl(-)/1H(+) antiporter highly expressed in endosomes of proximal tubule cells. It is essential for endocytosis and mutations in ClC-5 cause Dent's disease, potentially leading to renal failure. However, the physiological role of ClC-5 is still unclear. One
Miriam F Figueira et al.
Physiological reports, 5(13) (2017-07-06)
Diabetic nephropathy (DN) occurs in around 40% of those with diabetes. Proteinuria is the main characteristic of DN and develops as a result of increased permeability of the glomerulus capillary wall and/or decreased proximal tubule endocytosis. The goal of this
Ashish K Solanki et al.
Kidney international reports, 3(6), 1443-1453 (2018-11-15)
Tubular dysfunction is characteristic of Dent's disease; however, focal segmental glomerulosclerosis (FSGS) can also be present. Glomerulosclerosis could be secondary to tubular injury, but it remains uncertain whether the CLCN5 gene, which encodes an endosomal chloride and/or hydrogen exchanger, plays
Hengli Zhang et al.
Clinical & experimental optometry, 94(6), 528-535 (2011-09-08)
Experimental evidence has shown that myopic and hyperopic optical defocus induces thickening and thinning of the choroids, respectively, moving the retina forward and backward toward the plane of focus; however, the underlying mechanism of this phenomenon remains elusive. It has
Caroline M Gorvin et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(17), 7014-7019 (2013-04-11)
Receptor-mediated endocytosis, involving megalin and cubilin, mediates renal proximal-tubular reabsorption and is decreased in Dent disease because of mutations of the chloride/proton antiporter, chloride channel-5 (CLC-5), resulting in low-molecular-weight proteinuria, hypercalciuria, nephrolithiasis, and renal failure. To facilitate studies of receptor-mediated
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