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Merck
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主要文件

C1116

Sigma-Aldrich

Anti-Chloride Channel CLC-5 (Clcn5) antibody produced in rabbit

affinity isolated antibody, lyophilized powder

别名:

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

MDL號碼:
分類程式碼代碼:
12352203
NACRES:
NA.41
价格与库存信息目前不能提供

生物源

rabbit

品質等級

共軛

unconjugated

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

polyclonal

形狀

lyophilized powder

物種活性

human, mouse, rat

技術

western blot: 1:200 using rat kidney membranes

UniProt登錄號

運輸包裝

dry ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... CLCN5(1184)
mouse ... Clcn5(12728)
rat ... Clcn5(25749)

免疫原

peptide corresponding to amino acid residues 401-415 of rat CLC5. Mouse sequence is identical; human sequence is 14/15 residues identical.

應用

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.

生化/生理作用

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.

外觀

Lyophilized from phosphate buffered saline containing, pH 7.4, 1% BSA and 0.05% sodium azide

免責聲明

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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儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 2


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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
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
Amany A Azouz et al.
Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 30(2), 150-161 (2022-05-10)
Megalin receptor-mediated endocytosis participates a crucial role in gentamicin (GM) uptake, accumulation, and toxicity. In this study, we investigated the potential effects of montelukast (MLK) on megalin expression/endocytic function against GM nephrotoxicity. Male Wistar rats were administered GM (120 mg/kg; i.p.)

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