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  RNA editing of the IQ domain in cav1.3 channels modulates their ca2+-dependent inactivation

Huang, H., Tan, B. Z., Shen, Y., Tao, J., Jiang, F., Sung, Y. Y., et al. (2012). RNA editing of the IQ domain in cav1.3 channels modulates their ca2+-dependent inactivation. Neuron, 73(2), 304-316. doi:10.1016/j.neuron.2011.11.022.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-134D-8 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-1353-9
Genre: Journal Article
Alternative Title : RNA editing of the IQ domain in cav1.3 channels modulates their ca2+-dependent inactivation

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 Creators:
Huang, Hua1, Author              
Tan, Bao Zhen, Author
Shen, Yiru, Author
Tao, Jin, Author
Jiang, Fengli, Author
Sung, Ying Ying, Author
Ng, Choon Keow, Author
Raida, Manfred, Author
Köhr, Georg1, Author              
Higuchi, Miyoko1, Author              
Fatemi−Shariatpanahi, Hadi, Author
Harden, Bradley, Author
Yue, David T., Author
Soong, Tuck Wah, Author
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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 Abstract: Adenosine−to−inosine RNA editing is crucial for generating molecular diversity, and serves to regulate protein function through recoding of genomic information. Here, we discover editing within CaV1.3 Ca2+ channels, renown for low−voltage Ca2+−influx and neuronal pacemaking. Significantly, editing occurs within the channel's IQ domain, a calmodulin−binding site mediating inhibitory Ca2+−feedback (CDI) on channels. The editing turns out to require RNA adenosine deaminase ADAR2, whose variable activity could underlie a spatially diverse pattern of CaV1.3 editing seen across the brain. Edited CaV1.3 protein is detected both in brain tissue and within the surface membrane of primary neurons. Functionally, edited CaV1.3 channels exhibit strong reduction of CDI; in particular, neurons within the suprachiasmatic nucleus show diminished CDI, with higher frequencies of repetitive action−potential and calcium−spike activity, in wild−type versus ADAR2 knockout mice. Our study reveals a mechanism for fine−tuning CaV1.3 channel properties in CNS, which likely impacts a broad spectrum of neurobiological functions

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Title: Neuron
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 73 (2) Sequence Number: - Start / End Page: 304 - 316 Identifier: ISSN: 0896-6273
CoNE: https://pure.mpg.de/cone/journals/resource/954925560565