A5074768839- RNA Research and Splicing
- RNA and protein synthesis mechanisms
- RNA modifications and cancer
- Fungal and yeast genetics research
- RNA Interference and Gene Delivery
- 14-3-3 protein interactions
- Mitochondrial Function and Pathology
- Molecular Biology Techniques and Applications
- Cell Adhesion Molecules Research
- Genomics and Chromatin Dynamics
- Fungal Biology and Applications
- Microbial Natural Products and Biosynthesis
- Cancer-related gene regulation
- Microbial Metabolic Engineering and Bioproduction
- Cardiac electrophysiology and arrhythmias
- Plant and Fungal Interactions Research
- Lung Cancer Treatments and Mutations
- TGF-β signaling in diseases
- Electron Spin Resonance Studies
- Wnt/β-catenin signaling in development and cancer
- Lanthanide and Transition Metal Complexes
- Science, Research, and Medicine
- Fibroblast Growth Factor Research
- Heat shock proteins research
- Advanced NMR Techniques and Applications
Institute of Astronomy and Space Physics
2013
University of Oxford
2006
Genomics (United Kingdom)
2006
Fundación Ciencias Exactas y Naturales
1996-2003
Harvard University
1990-2002
University of Buenos Aires
1996-1999
International Centre for Genetic Engineering and Biotechnology
1997
Brigham and Women's Hospital
1990
It has been assumed that constitutive and regulated splicing of RNA polymerase II transcripts depends exclusively on signals present in the molecule. Here we show changes promoter structure strongly affect splice site selection. We investigated ED I exon, which encodes a facultative type III repeat fibronectin, whose inclusion is during development proliferative processes. used an alternative assay combined with swapping to demonstrate extent dependent from transcript originated this...
Promoter and enhancer elements can influence alternative splicing, but the basis for this phenomenon is not well understood. Here we investigated how different transcriptional activators affect decision between inclusion exclusion (skipping) of fibronectin EDI exon. A mutant acidic VP16 activation domain called SW6 that preferentially inhibits polymerase II (pol II) elongation caused a reduction in exon skipping. Exon skipping was fully restored presence by either SV40 cis or human...