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Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors.
Science. 1994 Sep 16; 265(5179):1706-9.Sci

Abstract

The opposing effects of SF2/ASF and heterogeneous nuclear ribonucleoprotein (hnRNP) A1 influence alternative splicing in vitro. SF2/ASF or hnRNP A1 complementary DNAs were transiently overexpressed in HeLa cells, and the effect on alternative splicing of several cotransfected reporter genes was measured. Increased expression of SF2/ASF activated proximal 5' splice sites, promoted inclusion of a neuron-specific exon, and prevented abnormal exon skipping. Increased expression of hnRNP A1 activated distal 5' splice sites. Therefore, variations in the intracellular levels of antagonistic splicing factors influence different modes of alternative splicing in vivo and may be a natural mechanism for tissue-specific or developmental regulation of gene expression.

Authors+Show Affiliations

Cold Spring Harbor Laboratory, NY 11724.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8085156

Citation

Cáceres, J F., et al. "Regulation of Alternative Splicing in Vivo By Overexpression of Antagonistic Splicing Factors." Science (New York, N.Y.), vol. 265, no. 5179, 1994, pp. 1706-9.
Cáceres JF, Stamm S, Helfman DM, et al. Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors. Science. 1994;265(5179):1706-9.
Cáceres, J. F., Stamm, S., Helfman, D. M., & Krainer, A. R. (1994). Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors. Science (New York, N.Y.), 265(5179), 1706-9.
Cáceres JF, et al. Regulation of Alternative Splicing in Vivo By Overexpression of Antagonistic Splicing Factors. Science. 1994 Sep 16;265(5179):1706-9. PubMed PMID: 8085156.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors. AU - Cáceres,J F, AU - Stamm,S, AU - Helfman,D M, AU - Krainer,A R, PY - 1994/9/16/pubmed PY - 1994/9/16/medline PY - 1994/9/16/entrez SP - 1706 EP - 9 JF - Science (New York, N.Y.) JO - Science VL - 265 IS - 5179 N2 - The opposing effects of SF2/ASF and heterogeneous nuclear ribonucleoprotein (hnRNP) A1 influence alternative splicing in vitro. SF2/ASF or hnRNP A1 complementary DNAs were transiently overexpressed in HeLa cells, and the effect on alternative splicing of several cotransfected reporter genes was measured. Increased expression of SF2/ASF activated proximal 5' splice sites, promoted inclusion of a neuron-specific exon, and prevented abnormal exon skipping. Increased expression of hnRNP A1 activated distal 5' splice sites. Therefore, variations in the intracellular levels of antagonistic splicing factors influence different modes of alternative splicing in vivo and may be a natural mechanism for tissue-specific or developmental regulation of gene expression. SN - 0036-8075 UR - https://www.unboundmedicine.com/medline/citation/8085156/Regulation_of_alternative_splicing_in_vivo_by_overexpression_of_antagonistic_splicing_factors_ L2 - https://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=8085156 DB - PRIME DP - Unbound Medicine ER -