IndraLab

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CACNA1H inhibits calcium(2+). 7 / 7
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"Since Cav3.2 is important in development and differentiation of ventricular myocytes, we also want to mention the possibility that Cav3.2 KO may alter the expression levels of EC-coupling proteins such as RyR or their cluster structure.Taken together, functional T-type Ca channels are expressed in ventricular cardiomyocytes of the working myocardium of healthy adult mice, and the lack of Cav3.2 channels impairs cellular Ca handling."
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"Previous studies have shown that mutations in CACNA1H disrupt Ca voltage-gated channels, leading to neural hyperexcitability and seizure occurrence."
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"For example, rare missense SNP mutations have been identified in the voltage dependent calcium channel gene CACNA1H (T-type Ca v 3.2), which reduce Ca v 3.2 channel activity."
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"A rare CACNA1H variant associated with amyotrophic lateral sclerosis causes complete loss of Ca v 3.2T-type channel activity."
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"Finally, Cav3.2 and TRPV3 double KO have shown decreased fertility, altered oocyte ER Ca dynamics (fill and re-fill), and severely impaired Ca oscillations in response to fertilization (Mehregan et al., 2021)."
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"Silencing Cacna1h significantly reduced Cacna1h protein levels ( Figure 3 F), eliminated T-type Ca 2+ currents ( Figure 3 G), and disabled COCH neurons to fire bursts of action potentials ( Figure 3 H[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Inhibition of Cacna1h transcription by MTF1 ΔCGFP was evidenced by reducing Cacna1h mRNA and protein levels ( Figure 4 D), eliminated T-type Ca 2+ currents ( Figure S6 A) and blocking the bursts of ac[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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