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CLCN2 Antibody (C-term) Blocking Peptide

Synthetic peptide

     
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Product Information
Primary Accession P51788
Clone Names 2021809
Additional Information
Gene ID 1181
Other Names Chloride channel protein 2, ClC-2, CLCN2
Target/Specificity The synthetic peptide sequence used to generate the antibody AP6329a was selected from the C-term region of human CLCN2. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
Format Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name CLCN2
Function Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume, membrane potential stabilization, signal transduction and transepithelial transport. Involved in the regulation of aldosterone production. The opening of CLCN2 channels at hyperpolarized membrane potentials in the glomerulosa causes cell membrane depolarization, activation of voltage- gated Ca2+ channels and increased expression of aldosterone synthase, the rate-limiting enzyme for aldosterone biosynthesis (PubMed:29403011, PubMed:29403012).
Cellular Location Cell membrane; Multi-pass membrane protein
Tissue Location Ubiquitously expressed. Moderately expressed in aortic and coronary vascular smooth muscle cells and expressed at a low level in aortic endothelial cells. Expressed in the adrenal gland, predominantly in the zona glomerulosa (PubMed:29403011)
Research Areas
Citations (0)
citation

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Background

CLCN2 is a voltage-gated chloride channel, a class of proteins that have several functions including the regulation of cell volume, membrane potential stabilization, signal transduction and transepithelial transport. This protein is ubiquitously expressed, with moderate expression in aortic and coronary vascular smooth muscle cells and low levels expressed in aortic endothelial cells. Defects in CLCN2 may be the cause of epilepsy with grand mal seizures on awakening, childhood absence epilepsy type 3, and juvenile absence epilepsy. Single nucleotide polymorphisms (SNPs) of CLCN2 may also at as potential modifiers of cystic fibrosis disease severity.

References

Hum. Molec. Genet. 4: 407-413, 1995. Nature Genet. 33: 527-532, 2003. Hum. Molec. Genet. 9: 1465-1472, 2000.Proc. Nat. Acad. Sci. 95: 3879-3884, 1998. Neuroscience. 101: 51-65, 2000.Biochem. Biophys. Res. Commun. 95, 265-271 (2005)

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$ 277.78
Cat# BP6329a
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