{'fraction_non_alphanumeric': 0.05053191489361702, 'fraction_numerical': 0.013297872340425532, 'mean_word_length': 5.3277310924369745, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pathophysiological significance of T-type Ca2+ channels: transcriptional regulation of T-type Ca2+ channel--regulation of CACNA1H by neuron-restrictive silencer factor.

Expression of T-type Ca(2+) current in the ventricle varies during development and in cardiac diseases. The alteration in quantity of two isoforms of T-type Ca(2+) channel genes in the heart, CACNA1G and CACNA1H, contributes to the changes of T-type Ca(2+) channel activity. However, the precise mechanisms governing the transcription of T-type Ca(2+) channel genes remain largely unknown. In this review, we briefly describe our recent finding that a transcriptional repressor named neuron-restrictive silencer factor is a potent regulator of T-type Ca(2+) channel gene expression.