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RNAi-mediated PTB depletion leads to enhanced exon definition.
Mol Cell. 2002 Oct; 10(4):943-9.MC

Abstract

Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo.

Authors+Show Affiliations

Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

12419237

Citation

Wagner, Eric J., and Mariano A. Garcia-Blanco. "RNAi-mediated PTB Depletion Leads to Enhanced Exon Definition." Molecular Cell, vol. 10, no. 4, 2002, pp. 943-9.
Wagner EJ, Garcia-Blanco MA. RNAi-mediated PTB depletion leads to enhanced exon definition. Mol Cell. 2002;10(4):943-9.
Wagner, E. J., & Garcia-Blanco, M. A. (2002). RNAi-mediated PTB depletion leads to enhanced exon definition. Molecular Cell, 10(4), 943-9.
Wagner EJ, Garcia-Blanco MA. RNAi-mediated PTB Depletion Leads to Enhanced Exon Definition. Mol Cell. 2002;10(4):943-9. PubMed PMID: 12419237.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - RNAi-mediated PTB depletion leads to enhanced exon definition. AU - Wagner,Eric J, AU - Garcia-Blanco,Mariano A, PY - 2002/11/7/pubmed PY - 2002/11/26/medline PY - 2002/11/7/entrez SP - 943 EP - 9 JF - Molecular cell JO - Mol Cell VL - 10 IS - 4 N2 - Mutually exclusive use of exons IIIb or IIIc in FGF-R2 transcripts requires the silencing of exon IIIb. This repression is mediated by silencer elements upstream and downstream of the exon. Both silencers bind the polypyrimidine tract binding protein (PTB) and PTB binding sites within these elements are required for efficient silencing of exon IIIb. Recruitment of MS2-PTB fusion proteins upstream or downstream of exon IIIb causes repression of this exon. Depletion of endogenous PTB using RNAi increases exon IIIb inclusion in transcripts derived from minigenes and from the endogenous FGF-R2 gene. These data demonstrate that PTB is a negative regulator of exon definition in vivo. SN - 1097-2765 UR - https://www.unboundmedicine.com/medline/citation/12419237/RNAi_mediated_PTB_depletion_leads_to_enhanced_exon_definition_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1097-2765(02)00645-7 DB - PRIME DP - Unbound Medicine ER -