Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
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Contact

 

+44 (0)013 34621727m.d.schneider Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Kirshenbaum:1995:10.1074/jbc.270.14.7791,
author = {Kirshenbaum, LA and Schneider, MD},
doi = {10.1074/jbc.270.14.7791},
journal = {J Biol Chem},
pages = {7791--7794},
title = {Adenovirus E1A represses cardiac gene transcription and reactivates DNA synthesis in ventricular myocytes, via alternative pocket protein- and p300-binding domains.},
url = {http://dx.doi.org/10.1074/jbc.270.14.7791},
volume = {270},
year = {1995}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - To examine the potential impact of disrupting "pocket" protein function on cardiac differentiation and growth, we introduced 12 S E1A genes into neonatal ventricular myocytes, by adenoviral gene transfer. In the absence of E1B, E1A was cytotoxic, with features typical of apoptosis. In the presence of E1B, E1A preferentially inhibited transcription of cardiac-restricted alpha-actin promoters, and reactivated DNA synthesis in cardiac myocytes, without cell death. Mutations that abrogate known activities of the amino terminus of E1A, versus conserved region 2, demonstrate that the "pocket" protein- and p300-binding domains each suffice, in the absence of the other, for transcriptional repression and re-entry into S phase.
AU - Kirshenbaum,LA
AU - Schneider,MD
DO - 10.1074/jbc.270.14.7791
EP - 7794
PY - 1995///
SN - 0021-9258
SP - 7791
TI - Adenovirus E1A represses cardiac gene transcription and reactivates DNA synthesis in ventricular myocytes, via alternative pocket protein- and p300-binding domains.
T2 - J Biol Chem
UR - http://dx.doi.org/10.1074/jbc.270.14.7791
UR - https://www.ncbi.nlm.nih.gov/pubmed/7713869
VL - 270
ER -