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Validated All-in-One™ qPCR Primer for HCN4(NM_005477.2) Search again
Product ID:
HQP000040
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BRGDA8, EIG18, SSS2
Gene Description:
hyperpolarization activated cyclic nucleotide gated potassium channel 4
Target Gene Accession:
NM_005477.2(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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Summary
This gene encodes a member of the hyperpolarization-activated cyclic nucleotide-gated potassium channels. The encoded protein shows slow kinetics of activation and inactivation, and is necessary for the cardiac pacemaking process.
Gene References into function
- The rat HCN1 and HCN4 were shown to mediate responses to sour stimuli, suggesting a potential new function for the related human proteins.
- HCN4 activates substantially slower than HCN2 and with a half-maximum activation voltage approximately equal 10 mV less negative, both isoforms activate more positively in myocytes suggesting cell-type specificity
- A heterozygous 1-bp deletion (1631delC) in exon 5 of the human HCN4 gene was detected in a patient with idiopathic sinus bradycardia and chronotropic incompetence
- the speed of activation of the HCN4 channel is determined by structural elements present in the S1, S1-S2 linker, and the S2 segment
- co-expressed KCNE2 enhanced HCN4-generated current amplitudes, slowed the activation kinetics and shifted the voltage for half-maximal activation of currents to more negative voltages
- A mouse model for a loss-of-function study of HCN4, which has a strong implication for the function of the related human protein.
- Data suggest that the loss of function of HCN4 is associated with sinus nodal dysfunction.
- Native I(f) channels in atrial myocardium are heteromeric complexes composed of HCN4 and/or HCN2.
- Sinus bradycardia in members of a large family was associated with a mutation in the gene coding for the pacemaker HCN4 ion channel.
- With computer modelling, we show that in channels with relatively slow opening kinetics and fast mode-shift transitions, such as HCN2 and HCN4 channels, the mode shift effects are not readily observable, except in the tail kinetics.
- A missense mutation, G480R, in the ion channel pore domain caused sinus node dysfunction. Mutant HCN4 had reduced synthesis, was activated at more negative voltages, & had defective ion trafficking.
- Src tyrosine kinase enhances HCN4 currents by shifting their activation to more positive potentials and increasing the whole cell channel conductance as well as speeding the channel kinetics. Tyr(531) mediates most of Src's actions on HCN4 channels.
- down-regulation of miR-1 and miR-133 expression contributes to re-expression of HCN2/HCN4 and thereby the electrical remodeling process in hypertrophic hearts
- HCN4 associates with Cav3 to form a HCN4 macromolecular complex. Our results also indicated that disruption of caveolae using P104L alters HCN4 function and could cause a reduction of cardiac pacemaker activity.