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Validated All-in-One™ qPCR Primer for KCNJ2(NM_000891.2) Search again
Product ID:
HQP010003
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ATFB9, HHBIRK1, HHIRK1, IRK1, KIR2.1, LQT7, SQT3
Gene Description:
potassium inwardly rectifying channel subfamily J member 2
Target Gene Accession:
NM_000891.2(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
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses.
Gene References into function
- molecular cloning from and conductance in nasal mucosal epithelium
- Modulation of the inward rectifier potassium channel IRK1 by the Ras signaling pathway
- Heteromerization of Kir2.1 channel contributes to the phenotype of Andersen syndrome
- Thr192Ala missense mutation found in familial periodic paralysis with ventricular dysrhythmia and marked QT prolongation
- KCNJ2 mutation results in Andersen syndrome with sex-specific cardiac and skeletal muscle phenotypes
- Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome)
- effect of suppressing excitability in single neurons within a network of active hippocampal neurons by overexpressing an inward-rectifier potassium channel
- expression of Kir2.1 protein in proliferative smooth muscle cells, consistent with the higher current density
- filamin-A was found to have no effect on Kir2.1 channel behavior but, rather, increased the number of functional channels resident within the membrane
- the small GTPase, Rho, transduces the m1 muscarinic receptor-induced inhibition of Kir2.1 via an unidentified mechanism.
- data show that the Andersen-Tawil syndrome phenotype may occur through a dominant-negative effect as well as through haplo-insufficiency and reveal amino acids critical in trafficking and conductance of the inward rectifier K+ channels.
- Kir2.1 channel activation is a required key early event that initiates myogenesis by turning on myogenin and MEF2 transcription factors via a hyperpolarization-activated Ca(2+)-dependent pathway
- Coexpression of Kir2.1 and PSD-93delta had no discernible effect upon channel kinetics but resulted in cell surface Kir2.1 clustering and suppression of channel internalization.
- Data describe the construction of a new cell line stably expressing alpha(1G) and Kir2.1 subunits in HEK293 cells.
- The present results suggest that the outward I(K1) flows through two populations of Kir2.1 channels with different sensitivities to cytoplasmic blockers.
- Consequently, the steady-state voltage dependence of IRK1 block by spermine or bis-QA(C10) should increase with membrane depolarization, a prediction indeed observed.
- Andersen's syndrome-associated mutations and hypokalaemic periodic paralysis-associated calcium channel mutations may lead to muscle membrane hypoexcitability via a common mechanism
- Kir2.1 gain-of-function mutation may have a role in development of familial atrial fibrillation
- Kir2.2 and Kir2.1 are primary determinants of endogenous K(+) conductance in HAECs under resting conditions and that Kir2.2 provides the dominant conductance in these cells.
- Results describe the regulation of inwardly rectifying potassium current and its main molecular correlates, Kir2.1, Kir2.2 and Kir2.3 channels, by endothelin-1 in human atrial cardiomyocytes.
- In conclusion, the data are consistent with the universal mechanism of rectification in Kir2 channels, but also point to significant, and physiologically important, quantitative differences between Kir2 isoforms.
- Results suggest that chronic exposure to certain drugs and their effects on Kir2.1 and ERG potassium channels may be an important aspect of acquired QT prolongation.
- Mutations in KCNJ2 is associated with Andersen-Tawil syndrome
- The cytoplasmic pore of Kir electrostatically gathers cations such as Mg(2+), spermine, and K(+) so that the transmembrane pore is sufficiently filled with K(+) ions, which enables strong voltage-dependent blockade with adequate outward K(+) conductance.
- The results demonstrate functional consequences of two novel trafficking-competent KCNJ2 mutations associated with Andersen syndrome.
- Kir2.1 had a strong dominant negative effect in the Xenopus oocyte expression system. The T75R-Transgenic mice had bidirectional ventricular tachycardia after induction and longer QT intervals.
- These results establish the direct regulation of Kir channels by the cytoplasmic accumulation of LC-CoA, which might be of physiological and pathophysiological relevance in a variety of tissues.
- Kir2.1-induced hyperpolarization triggers human myoblast differentiation via the activation of the calcineurin pathway, which, in turn, induces expression/activity of myogenin and MEF2.
- Individual Andersen's Syndrome mutations R218Q, G300V, E303K, and delta314-315 affecting the ability of the cytoplasmic domains in Kir2.1 channels to form proper tetrameric assemblies were characterised.
- Co-expression of Kir2.1 changes the pattern of subcellular distribution of GRIF-1.
- We demonstrated that 9.5% of cases diagnosed as SIDS carry functionally significant genetic variants in LQTS genes (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2, KCNJ2, CAV3).
- Two missense mutations of KCNJ2 (R218Q and M307I) are identified in two Korean families diagnosed with Andersen-Tawil syndrome.
- Novel Kir2.1 mutations at residues C54 and T305 linked to Andersen Syndrome.
- KCNJ2 loss of function mutations were found in approximately 1% of patients referred for genetic arrhythmia testing that lacked criteria for Andersen-Tawil Syndrome.
- These findings suggest that non-syndromic PRS may be caused by both SOX9 and KCNJ2 dysregulation.
- The T75M mutation caused alteration of gating kinetics of the mutated KCNJ2 channels, i.e., increased sensitivity to intracellular Mg2+ and resultant enhancement of inward rectification.
- results suggest that 1 negative charge of D152 or 2 negative charges of E153 are required for Kir2.1 channels to function. contribution by D152 & E153 to the electronegative extracellular pore entrance is critical for the channel to function properly.
- Modulation of the outward Kir2.1 current alters tone and calcium signaling in the afferent arterioles but not in the efferent arterioles of kidneys.
- We conclude that the lysosomal degradation pathway contributes to Kir2.1 mediated inward rectifier current regulation.
- Kir2.1 channels are already present at the membrane of proliferating, undifferentiated human myoblasts but in a silent state, and Kir2.1 tyrosine 242 dephosphorylation triggers differentiation.
- Report exaggerated Mg2+ inhibition of Kir2.1 as a consequence of reduced PIP2 sensitivity in Andersen syndrome.
- Kir2.1 exhibits a clear and temporal expression in the hair cells of mouse cochleae which may be related to the functional maturation of the hair cells and the neurons.