Please use this identifier to cite or link to this item:
https://doi.org/10.1523/JNEUROSCI.2093-06.2006
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dc.title | Alternative splicing of the Ca V1.3 channel IQ domain, a molecular switch for Ca 2+-dependent inactivation within auditory hair cells | |
dc.contributor.author | Shen, Y. | |
dc.contributor.author | Yu, D. | |
dc.contributor.author | Hiel, H. | |
dc.contributor.author | Liao, P. | |
dc.contributor.author | Yue, D.T. | |
dc.contributor.author | Fuchs, P.A. | |
dc.contributor.author | Tuck, W.S. | |
dc.date.accessioned | 2014-11-26T07:42:38Z | |
dc.date.available | 2014-11-26T07:42:38Z | |
dc.date.issued | 2006-10-18 | |
dc.identifier.citation | Shen, Y., Yu, D., Hiel, H., Liao, P., Yue, D.T., Fuchs, P.A., Tuck, W.S. (2006-10-18). Alternative splicing of the Ca V1.3 channel IQ domain, a molecular switch for Ca 2+-dependent inactivation within auditory hair cells. Journal of Neuroscience 26 (42) : 10690-10699. ScholarBank@NUS Repository. https://doi.org/10.1523/JNEUROSCI.2093-06.2006 | |
dc.identifier.issn | 02706474 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/109165 | |
dc.description.abstract | Native Ca V1.3 channels within cochlear hair cells exhibit a surprising lack of Ca 2+-dependent inactivation (CDI), given that heterologously expressed Ca V1.3 channels show marked CDI. To determine whether alternative splicing at the C terminus of the Ca V1.3 gene may produce a hair cell splice variant with weak CDI, we transcript-scanned mRNA obtained from rat cochlea. We found that the alternate use of exon 41 acceptor sites generated a splice variant that lost the calmodulin-binding IQ motif of the C terminus. These Ca V1.3 IQΔ ("IQ deleted") channels exhibited a lack of CDI, which was independent of the type of coexpressed β-subunits. Ca V1.3 IQΔ channel immunoreactivity was preferentially localized to cochlear outer hair cells (OHCs), whereas that of Ca V1.3 IQfull channels (IQ-possessing) labeled inner hair cells (IHCs). The preferential expression of Ca V1.3 IQΔ within OHCs suggests that these channels may play a role in processes such as electromotility or activity-dependent gene transcription rather than neurotransmitter release, which is performed predominantly by IHCs in the cochlea. Copyright © 2006 Society for Neuroscience. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1523/JNEUROSCI.2093-06.2006 | |
dc.source | Scopus | |
dc.subject | Alternative splicing | |
dc.subject | Calcium channels | |
dc.subject | Calcium-dependent inactivation | |
dc.subject | Hair cells | |
dc.subject | L-type calcium channels | |
dc.subject | Splice variant | |
dc.type | Article | |
dc.contributor.department | PHYSIOLOGY | |
dc.description.doi | 10.1523/JNEUROSCI.2093-06.2006 | |
dc.description.sourcetitle | Journal of Neuroscience | |
dc.description.volume | 26 | |
dc.description.issue | 42 | |
dc.description.page | 10690-10699 | |
dc.description.coden | JNRSD | |
dc.identifier.isiut | 000241727300012 | |
Appears in Collections: | Staff Publications |
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