Skip to main content
Journal cover image

Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells.

Publication ,  Journal Article
Bertolesi, GE; Walia Da Silva, R; Jollimore, CAB; Shi, C; Barnes, S; Kelly, MEM
Published in: Neuroscience
August 11, 2006

A decrease in transient-type calcium channel current, Ca(v)3.1 protein and the mRNA encoding these channels has been reported during differentiation of human retinoblastoma cells. In this study, we examined splice variants of Ca(v)3.1 before and after neuronal differentiation of the Y-79 retinoblastoma cell line to investigate the potential contribution of Ca(v)3.1 to Y-79 differentiation. In Ca(v)3.1, alternative splicing induces variations in three cytoplasmic regions, e.g. the link between domains II and III (producing isoforms e+ and e-), the link between domains III and IV (producing isoforms a, b, ac and bc) and the carboxy terminal region (producing isoforms f and d). Our results demonstrate that Ca(v)3.1e was not expressed in either undifferentiated or differentiated retinoblastoma cells. Splice variants Ca(v)3.1ac; Ca(v)3.1bc and Ca(v)3.1b were all identified in undifferentiated retinoblastoma cells, while expression of these variants in differentiated cells was restricted to the Ca(v)3.1bc isoform. The carboxy terminal variant Ca(v)3.1f is expressed independently of the differentiation status of retinoblastoma cells with or without Ca(v)3.1d. Examination of the functional contribution of Ca(v)3.1 protein to Y-79 cell differentiation revealed that in Y-79 cells transfected with Ca(v)3.1 antisense oligodeoxynucleotides, knockdown of Ca(v)3.1 did not alter the time-course of differentiation or neuritogenesis. The changes in Ca(v)3.1 splice variants were not required for the initiation of differentiation but may be associated with tissue-specific expression or localized alterations in Ca(2+) signaling that are essential for establishment of the mature differentiated phenotype.

Duke Scholars

Published In

Neuroscience

DOI

ISSN

0306-4522

Publication Date

August 11, 2006

Volume

141

Issue

1

Start / End Page

259 / 268

Location

United States

Related Subject Headings

  • Tubulin
  • Transfection
  • Time Factors
  • Reverse Transcriptase Polymerase Chain Reaction
  • Retinoblastoma
  • RNA, Messenger
  • Patch-Clamp Techniques
  • Neurons
  • Neurology & Neurosurgery
  • Models, Molecular
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Bertolesi, G. E., Walia Da Silva, R., Jollimore, C. A. B., Shi, C., Barnes, S., & Kelly, M. E. M. (2006). Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells. Neuroscience, 141(1), 259–268. https://doi.org/10.1016/j.neuroscience.2006.03.067
Bertolesi, G. E., R. Walia Da Silva, C. A. B. Jollimore, C. Shi, S. Barnes, and M. E. M. Kelly. “Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells.Neuroscience 141, no. 1 (August 11, 2006): 259–68. https://doi.org/10.1016/j.neuroscience.2006.03.067.
Bertolesi GE, Walia Da Silva R, Jollimore CAB, Shi C, Barnes S, Kelly MEM. Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells. Neuroscience. 2006 Aug 11;141(1):259–68.
Bertolesi, G. E., et al. “Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells.Neuroscience, vol. 141, no. 1, Aug. 2006, pp. 259–68. Pubmed, doi:10.1016/j.neuroscience.2006.03.067.
Bertolesi GE, Walia Da Silva R, Jollimore CAB, Shi C, Barnes S, Kelly MEM. Ca(v)3.1 splice variant expression during neuronal differentiation of Y-79 retinoblastoma cells. Neuroscience. 2006 Aug 11;141(1):259–268.
Journal cover image

Published In

Neuroscience

DOI

ISSN

0306-4522

Publication Date

August 11, 2006

Volume

141

Issue

1

Start / End Page

259 / 268

Location

United States

Related Subject Headings

  • Tubulin
  • Transfection
  • Time Factors
  • Reverse Transcriptase Polymerase Chain Reaction
  • Retinoblastoma
  • RNA, Messenger
  • Patch-Clamp Techniques
  • Neurons
  • Neurology & Neurosurgery
  • Models, Molecular