Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
//

Contact

 

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

 
 
//

Location

 

ICTEM buildingHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Abdellatif:1994,
author = {Abdellatif, M and MacLellan, WR and Schneider, MD},
journal = {J Biol Chem},
pages = {15423--15426},
title = {p21 Ras as a governor of global gene expression.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/8195182},
volume = {269},
year = {1994}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - The molecular mechanisms for signaling by receptor serine/threonine kinases are incompletely understood. To test the potential involvement of p21 H-Ras proteins in signal transduction for type beta transforming growth factors (TGF beta), TGF beta-responsive and constitutive reporter genes were cotransfected into cardiac myocytes and mink lung epithelial cells, with dominant inhibitory (Asn-17) or activated (Arg-12) Ras expression vectors. Asn-17 Ras inhibited both TGF beta-dependent and basal expression of inducible promoters (skeletal alpha-actin and plasminogen activator inhibitor-1), with equivalent dose-response relations. All seven reporter constructs were comparably sensitive to down-regulation by Asn-17 Ras, including those driven by nominally constitutive viral control regions or a TATA-less initiator element. All constructs were up-regulated by Arg-12 Ras more variably. Wild-type Ras had intermediate effects and could rescue a minimal thymidine kinase promoter from inhibition by dominant negative Ras. Thus, a Ras-dependent event is required for efficient expression of an unexpectedly global or inclusive set of genes.
AU - Abdellatif,M
AU - MacLellan,WR
AU - Schneider,MD
EP - 15426
PY - 1994///
SN - 0021-9258
SP - 15423
TI - p21 Ras as a governor of global gene expression.
T2 - J Biol Chem
UR - https://www.ncbi.nlm.nih.gov/pubmed/8195182
VL - 269
ER -