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Antisense oligonucleotides against rat brain alpha1E DNA and its atrial homologue decrease T-type calcium current in

E S Piedras-Rentería1, C C Chen, P M Best

  • 1Department of Molecular and Integrative Physiology, University of Illinois, Urbana, IL 61801, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 7, 1998
PubMed
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Researchers identified a gene related to E class calcium channels that encodes low voltage-activated (T-type) calcium currents in atrial myocytes. This finding helps understand neuronal and muscle excitability regulation.

Area of Science:

  • Molecular biology
  • Cardiology
  • Neuroscience

Background:

  • Low voltage-activated, or T-type, calcium currents are crucial for neuronal and muscle excitability, secretion, and potentially cell growth.
  • The specific gene responsible for the pore-forming subunit of these channels remains unidentified.

Purpose of the Study:

  • To identify the gene encoding the low voltage-activated calcium channel in rat atrial myocytes.
  • To investigate the role of a specific calcium channel gene (raE1) in T-type current regulation.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) was used to identify partial gene clones from rat atrial myocytes.
  • Antisense oligonucleotides were employed to block specific gene sequences and observe effects on T-type calcium currents.

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Main Results:

  • Partial clones with high homology to the E class calcium channel gene (raE1) were identified in atrial myocytes.
  • Antisense oligonucleotides targeting raE1 and neuronal alpha1E sequences blocked insulin-like growth factor 1 (IGF-1)-induced increases in T-current.
  • Basal T-current was also blocked by antisense oligonucleotides, suggesting IGF-1 up-regulates the same gene.

Conclusions:

  • A member of the E class of calcium channel genes likely encodes the low voltage-activated calcium channel in atrial myocytes.
  • These findings support the hypothesis that raE1 or a closely related gene is responsible for T-type calcium currents in these cells.