IndraLab

Statements

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"This suggested that the loss of cAMP-controlled modulation of TREK1 currents was in part responsible for the cardiac arrhythmias observed in patients possessing the POPDC1 mutation and corresponding animal models [14]."
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"Interestingly, cAMP analogs have been reported to enhance TREK1 mRNA independently from PKA in adrenocortical cells XREF_BIBR."
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"However, in the case of rhythmic behavior such as the one observed for Ca transients, cAMP enhances the activity of TREK potassium channels that favors refractory periods preventing activity in starburst amacrine cells ."
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"In vitro experiments have shown how this POPDC1 S201F mutation, located in the cAMP binding site of POPDC1, causes an impaired cAMP-dependent suppression of TREK-1 that results in increased TREK-1 cur[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Since the retraction response of retinal axons exposed to ephrin-A5 requires electrical activity , a reduction in cAMP might prevent TREK channels activation and release the possibility of voltage-dependent Ca channel opening, thus leading to a rhythmic Ca transient activity."
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"Interestingly, as outlined in Table 5, a vast majority of identified binding and reaction partners of AKAP5 is altered in BD, being either up-regulated (cAMP dependent protein kinase A and its regulat[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The sAHP is generated by calcium dependent decay of cAMP which activates TREK1 potassium channels."
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"Thus, the impaired cAMP-dependent suppression of TREK-1 by POPDC1 S201F results in increased TREK-1 currents that might hyperpolarize cells of the atrium and/or conduction system, leading to an atrio-[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In addition, cAMP was supposed to negatively modulate the interaction of TREK-1 with POPDC proteins."
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