Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/109165
Title: Alternative splicing of the Ca V1.3 channel IQ domain, a molecular switch for Ca 2+-dependent inactivation within auditory hair cells
Authors: Shen, Y.
Yu, D.
Hiel, H.
Liao, P.
Yue, D.T.
Fuchs, P.A.
Tuck, W.S. 
Keywords: Alternative splicing
Calcium channels
Calcium-dependent inactivation
Hair cells
L-type calcium channels
Splice variant
Issue Date: 18-Oct-2006
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.
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.
Source Title: Journal of Neuroscience
URI: http://scholarbank.nus.edu.sg/handle/10635/109165
ISSN: 02706474
Appears in Collections:Staff Publications

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