CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cornwell, M. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cornwell, M. M.

Cell Growth & Differentiation, Vol 1, Issue 12 607-615, Copyright © 1990 by American Association of Cancer Research


ARTICLES

The human multidrug resistance gene: sequences upstream and downstream of the initiation site influence transcription

MM Cornwell
Department of Human Oncology, University of Wisconsin Medical School, Madison 53792.

To identify the DNA sequences required for multidrug resistance (MDR1) gene transcription, we have optimized conditions for transcription of the MDR1 proximal promoter in vitro. Using HeLa cell nuclear extracts, the direction, initiation, and RNA polymerase II dependence of transcription in vitro accurately reflect events in cells. The DNA template concentration, reaction temperature, and MgCl2 concentration were critical parameters of the in vitro system. Using conditions optimized for these parameters, the effect of deletions in the 5' flanking region and deletions in sequences downstream of the initiation site were examined. We found that deletion of sequences 5' and 3' of the transcription initiation site modulated the level of transcription. Of particular interest was the deletion of exon 1 sequences +5 to +127, which completely inhibited accurately initiated MDR1 transcription. Reconstitution of the +5 site, used for initiation in vivo and in vitro, did not reverse the inhibition. MDR1 transcription was specifically inhibited by an oligonucleotide corresponding to sequences +46 to +58. Our data indicate that sequences both upstream and downstream of the transcription initiation site modulate the efficiency of the MDR1 proximal promoter.


This article has been cited by other articles:


Home page
J. Virol.Home page
J. M. Bodily and C. Meyers
Genetic Analysis of the Human Papillomavirus Type 31 Differentiation-Dependent Late Promoter
J. Virol., March 15, 2005; 79(6): 3309 - 3321.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
D. G. Perez, C. Gomez, E. Lopez-Bayghen, E. Tannich, and E. Orozco
Transcriptional Analysis of the EhPgp5 Promoter of Entamoeba histolytica Multidrug-resistant Mutant
J. Biol. Chem., March 27, 1998; 273(13): 7285 - 7292.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
R. Sundseth, G. Macdonald, J. Ting, and A. C. King
DNA Elements Recognizing NF-Y and Sp1 Regulate the Human Multidrug-Resistance Gene Promoter
Mol. Pharmacol., June 1, 1997; 51(6): 963 - 971.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
M. E. Goldsmith, J. M. Gudas, E. Schneider, and K. H. Cowan
Wild Type p53 Stimulates Expression from the Human Multidrug Resistance Promoter in a p53-negative Cell Line
J. Biol. Chem., January 27, 1995; 270(4): 1894 - 1898.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1990 by the American Association of Cancer Research.