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1. |
We identified a group of markers occurring within the CACNA1C gene (encoding the alpha subunit of the calcium channel Cav1.2). |
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2. |
L-type calcium channel blockers exert an antiinflammatory effect by suppressing expression of plasminogen receptors on macrophages. |
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3. |
Overexpression of the intracellular II-III loop domains of Cav1.2 and Cav1.3 can dislodge the corresponding endogenous channels from the lipid raft regions of the membrane in rat insulinoma (INS-1) cells. |
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4. |
The structural organization of Ca(v)1.2 channels in the plasma membrane depends on the type of Ca(v)beta subunits present. |
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5. |
Three SNPs in CACNA1D or CACNA1C are genetic polymorphisms conferring sensitivity to the antihypertensive effects of L-type dCCBs in patients with hypertension. |
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6. |
Coupled and independent contributions of residues in IS6 and IIS6 to activation gating of CaV1.2. |
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7. |
Report functional properties of the CaV1.2 calcium channel activated by calmodulin in the absence of alpha2delta subunits. |
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8. |
Ca(V)1.2 channels are shown to be a mixture of monomers/dimers and a point mutation in the pre-IQ region predicted to abolish the coiled-coil structure significantly reduces Ca(2+)-dependent inactivation of heterologously expressed Ca(V)1.2 channels |
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9. |
Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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10. |
Introduction into Ca(v)2.1 of the homologous mutation of Ca(v)1.2 causing the Timothy syndrome questions the role of V421 in the phenotypic definition of P-type Ca(2+) channel. |
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11. |
activation of the RyR1 signaling cascade by Ca(v)1.2 may be important in the early stages of infection, providing the immune system with a rapid mechanism to initiate an early response |
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12. |
found further support for the previously reported CACNA1C (alpha 1C subunit of the L-type voltage-gated calcium channel in bipolar disorder |
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13. |
Sorcin modulates cardiac L-type Ca2+ current by functional interaction with the alpha1C subunit in rabbits. |
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14. |
CO, a product of heme catabolism by HO-1, directly inhibits alpha1C subunit of the cardiac L-type Ca2+ channel |
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15. |
Cav1.2 is subject to "denitration". |
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16. |
Observational study of gene-disease association. (HuGE Navigator) |
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17. |
Observational study and genome-wide association study of gene-disease association. (HuGE Navigator) |
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18. |
Coexpression of exogenous CaM (CaM(ex)) with alpha(1C)/alpha(2)delta in COS1 cells in the absence of Ca(v)beta subunits stimulates the plasma membrane targeting of alpha(1C). |
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19. |
Suggest that the decreased BAY K 8644 effects on Cav1.2 channels in failing cardiac myoyctes is caused by increased basal channel activity. |
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20. |
study found that the Timothy syndrome mutation powerfully and selectively slows voltage-dependent inactivation while sparing or possibly speeding the kinetics of calcium-dependent inactivation |
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21. |
Genome-wide association study of gene-disease association. (HuGE Navigator) |
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22. |
Observational study of gene-environment interaction and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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23. |
The COOH terminus of hCa(v)1.2b contains sites for the SH2 and SH3 binding of Src kinase. |
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24. |
Knckout mice mice exhibit significant impairments in spatial memory when examined 30 days after training. |
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25. |
a smooth muscle Ca(v)1.2 splice variant has been identified functionally to possess biophysical property that can be linked to enhanced state-dependent block by DHP |
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26. |
CS(L) modulates Ca2+-channel activity through interacting with the calmodulin-binding site on the C-terminal tail of the Cav1.2 channel. |
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27. |
Indirect evidence for an impaired src kinase regulation of I (Ca,L) together with an increased phosphatase activity suggests that a complex alteration in the kinase/phosphatase balance leads to I (Ca,L) dysregulation in chronic AF. |
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28. |
data indicate that gain-of-function mutations of CaV1.2 exons 8 and 8A cause distinct forms of Timothy syndrome |
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29. |
there are extensive splice variations in the human l-type voltage-gated calcium channel, Cav1.2 alpha1 subunit |
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30. |
testosterone inhibits currents in a concentration-dependent manner over the physiological range of testosterone concentrations (IC50 34 nM), and is not mimicked by the metabolite 5alpha-androstan-17beta-ol-3-one (DHT), nor by progesterone or estradiol. |
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31. |
the inhibitory modulation of cardiac Ca2+ channels, present in both alpha(1C) isoforms, is G(q)- and PLC-independent and Ca(2+)-dependent, but only basal levels of Ca(2+) are essential |
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32. |
Ahnak has a critical role in cardiac Ca(V)1.2 calcium channel function and its beta-adrenergic regulation |
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33. |
The high-resolution structure of the Ca(2+)/CaM-Ca(V)1.2 IQ domain complex was reported. |
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34. |
determination of whether the expression of this channel is regulated by different promoters in smooth muscle cells and in heart |
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35. |
there are multiple residues within the inhibitory domain that are crucial to the inhibitory process as well as to the enhancement of expressed current by intracellular application of proteases |
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36. |
Ca(2+)-calmodulin assumes a novel conformation when it is part of a complex with the C-terminal tail of the Ca(V)1.2 alpha(1) subunit |
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37. |
L-type Ca(2+) channels play a critical role in maintaining lower esophageal sphinctor tone. |
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38. |
Expression of undeleted L-type calcium channel mRNAs correlates with normal testes cadmium and increased sperm count after varicocelectomy |
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39. |
activation of Ca(2+) conductance and Ca(2+)-dependent inactivation depend on extracellular Ca(2+) and are linked to changes in selectivity |
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40. |
The activation of p50 and p65 by tumor necrosis factor alpha suppresses the expression of the alpha1C subunit of Cav1.2 channels in human colonic circular smooth muscle cells |
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41. |
single nucleotide polymorphisms in CANCA1C had significant associations with antihypertensive outcome, combining to yield a positive treatment outcome of less than 15 to 80% |
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42. |
functional but non-voltage-gated L-type Ca2+ channels are expressed at the plasma membrane in T cells and play a role in the antigen receptor-mediated Ca2+ flux in these cells |
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43. |
Timothy syndrome results from a Ca(V)1.2 missense mutation. Ca(V)1.2 is expressed in all affected tissues. Functional expression reveals that G406R produces maintained inward Ca(2+) currents by causing loss of voltage-dependent channel inactivation. |
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44. |
localized changes in cytokine expression generated by inflammation in atherosclerosis affect alternative splicing of the Ca(v)1.2alpha1 gene |
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45. |
loss-of-function mutations in genes encoding the cardiac L-type calcium channel to be associated with a familial sudden cardiac death syndrome in which a Brugada syndrome phenotype is combined with shorter-than-normal QT intervals |
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46. |
short splice variants of the human cardiac Cavbeta2 subunit are involved in modulation of the Cav1.2 channel |
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47. |
the NT and IQ-domains of alpha(1)1.2 mediate functionally distinct interactions with CaBP1 and CaM that promote conformational alterations that either stabilize or inhibit inactivation of Ca(v)1.2. |
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48. |
voltage-dependent facilitation of the Ca(v)1.2 channel depends on the phosphorylation of Ser1512/Ser1570 by calmodulin kinase II |
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49. |
cross-talk between the alpha1C C and N termini, beta subunit, and the cytoplasmic pore region confers the multifactorial regulation of Ca(v)1.2 channels |
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50. |
tissue-secific expression of two isoforms under the control of distinct 5' flanking regulatory elements |
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51. |
the physicochemical properties of the amino acid residues at positions 1144 and 1152 are crucial to the CaV1.2 pore's ability to distinguish between multiple Ba(2+) ions and Ca(2+) ions |
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52. |
analysis of conformation and binding of CaV1.2 |
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53. |
new promoter which exhibits 69% homology to its rat counterpart and displays functional promoter activity when transfected into heart cells in culture in luciferase-expressing constructs |
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54. |
We conclude that Rem is capable of regulating L-type current, that release of Rem block is modulated by cellular kinase pathways, and that the Ca(V)1.2 COOH terminus contributes to Rem-dependent channel inhibition. |