C1116
Anti-Chloride Channel CLC-5 (Clcn5) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonyme(s) :
Anti-CLC5, Anti-CLCK2, Anti-ClC-5, Anti-DENT1, Anti-DENTS, Anti-NPHL1, Anti-NPHL2, Anti-XLRH, Anti-XRN
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50 μL
291,00 €
200 μL
826,00 €
291,00 €
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Changer de vue
50 μL
291,00 €
200 μL
826,00 €
About This Item
291,00 €
Veuillez contacter notre Service Clients pour connaître la disponibilité de ce produit.
Produits recommandés
Source biologique
rabbit
Niveau de qualité
Conjugué
unconjugated
Forme d'anticorps
affinity isolated antibody
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
lyophilized powder
Espèces réactives
human, mouse, rat
Technique(s)
western blot: 1:200 using rat kidney membranes
Numéro d'accès UniProt
Conditions d'expédition
dry ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... CLCN5(1184)
mouse ... Clcn5(12728)
rat ... Clcn5(25749)
Immunogène
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.
Actions biochimiques/physiologiques
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.
Forme physique
Lyophilized from phosphate buffered saline containing, pH 7.4, 1% BSA and 0.05% sodium azide
Clause de non-responsabilité
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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Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 2
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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
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
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
Christina D'Antonio et al.
The Biochemical journal, 452(3), 391-400 (2013-04-10)
Mutations in the CLCN5 (chloride channel, voltage-sensitive 5) gene cause Dent's disease because they reduce the functional expression of the ClC-5 chloride/proton transporter in the recycling endosomes of proximal tubule epithelial cells. The majority (60%) of these disease-causing mutations in
Jonathan D Lippiat et al.
Frontiers in physiology, 3, 449-449 (2012-12-12)
CLC-5 plays a critical 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 I disease. In this X-linked disorder impaired reabsorption results in the wasting
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