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Validated All-in-One™ qPCR Primer for CLCN2(NM_004366.5) Search again
Product ID:
HQP001982
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CIC-2, CLC2, ECA2, ECA3, EGI11, EGI3, EGMA, EJM6, EJM8, FHA2, FHII, HALD2, LKPAT, clC-2
Gene Description:
chloride voltage-gated channel 2
Target Gene Accession:
NM_004366.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- found significant expression of ClC-2 at the apex of ciliated cells in both rat and human airways
- a functional interaction between the ClC-2 chloride channel and the retrograde motor dynein complex.
- the chloride-channel gene CLCN2 has a role in membrane depolarization and hyperexcitability, and its mutation may be a cause of generalized epilepsy
- ClC-2 and ClC-3 channels are specifically upregulated in glioma membranes and endow glioma cells with an enhanced ability to transport Chloride
- activation of hClC-2 is differentially regulated by PKA at two sites
- Functional evaluation of mutated channels associated with idiopathic generalized epilepsies
- activation of host ClC-2 channels participates in the altered permeability of Plasmodium-infected erythrocytes but is not required for intraerythrocytic parasite survival
- These results indicate that ClC-2 may not be a Cl- -transporting protein for gastric acid secretion in parietal cells.
- These data suggest that interferon-gamma activates ClC-2 channel activity in lung epithelial cells via mRNA stabilization.
- The authors conclude that CLCN2 mutations may be a rare cause of familial epilepsy. Further studies are needed to test if polymorphisms in this gene are associated with epilepsy.
- CLC-2 is not a key modifier gene of Cystic fibrosis lung disease phenotype.
- CLCN2 is related to idiopathic generalized epilepsy.
- association of Hsp90 with ClC-2 results in greater channel activity due to increased cell surface channel expression, facilitation of channel opening, and enhanced channel sensitivity to intracellular [Cl-]
- This suggests that slow and fast gating in ClC-2 are coupled, perhaps with slow gating contributing to the operation of the pore E207 as a protopore gate.
- mutations in the CLCN2 gene are only a rare cause of idiopathic generalized epilepsy
- CLCN2 may be a susceptibility locus in a subset of cases of childhood absence epilepsy
- Africans' gene pool comprises CLCN2 gene variants in the N-terminus, the C-terminus or the pore domain that affect surface expression and voltage- or cell-swelling-stimulated channel gating
- CLC-2 is upregulated in ethmoid mucosa and may affect the development of chronic rhinosinusitis without nasal polyps.
- propose that the function of the ClC-2 carboxy-terminus is to slow down the time course of channel activation in order to stabilize neuronal excitability