Mdr1b facilitates p53-mediated cell death and p53 is required for Mdr1b upregulation in vivo

The mdr1b gene is thought to be a "stress-responsive" gene, however it is unknown if this gene is regulated by p53 in the whole animal. Moreover, it is unknown if overexpression of mdr1b affects cell survival. The dependence of mdr1b upon p53 for upregulation was evaluated in p53 knockout...

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Veröffentlicht in:Oncogene 2001-01, Vol.20 (3), p.303-313
Hauptverfasser: LECUREUR, Valerie, THOTTASSERY, Jaideep V, DAXI SUN, SCHUETZ, Erin G, LAHTI, Jill, ZAMBETTI, Gerard P, SCHUETZ, John D
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container_issue 3
container_start_page 303
container_title Oncogene
container_volume 20
creator LECUREUR, Valerie
THOTTASSERY, Jaideep V
DAXI SUN
SCHUETZ, Erin G
LAHTI, Jill
ZAMBETTI, Gerard P
SCHUETZ, John D
description The mdr1b gene is thought to be a "stress-responsive" gene, however it is unknown if this gene is regulated by p53 in the whole animal. Moreover, it is unknown if overexpression of mdr1b affects cell survival. The dependence of mdr1b upon p53 for upregulation was evaluated in p53 knockout mice. Wild-type (wt) or p53-/- mice were treated singly or in combination with gamma irradiation (IR) and/or the potent DNA damaging agent, diethylnitrosoamine (DEN). Both IR and DEN induced mdr1b in wild-type animals, but not in the p53-/- mice. IR also upregulated endogenous mdr1b in the H35 liver cell line, and the mdr1b promoter was activated by IR and activation correlated with p53 levels; moreover activation required an intact p53 binding site. Colony survival studies revealed that co-transfection of both mdr1b and p53 dramatically reduced colony numbers compared to cells transfected with either p53 or mdr1b alone and cells microinjected with both mdr1b and p53 had a more dramatic loss in viability compared to cells injected with either expression vector alone. Further studies using acridine orange and ethidium bromide to measure apoptosis revealed that mdr1b caused apoptosis and this was enhanced by p53, however the increased apoptosis required a functional p53 transactivation domain. These studies indicate that mdr1b is a downstream target of p53 in the whole animal and expression of mdr1b facilitates p53-mediated cell death.
doi_str_mv 10.1038/sj.onc.1204065
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subjects Ageing, cell death
Alkylating Agents - pharmacology
Animals
ATP Binding Cassette Transporter, Subfamily B - genetics
ATP Binding Cassette Transporter, Subfamily B - metabolism
ATP Binding Cassette Transporter, Subfamily B - radiation effects
ATP-Binding Cassette Sub-Family B Member 4
Base Sequence
Binding Sites
Biological and medical sciences
Cell death
Cell Death - physiology
Cell physiology
Cells, Cultured
Conserved Sequence
Diethylnitrosamine - pharmacology
DNA Damage - drug effects
DNA Damage - genetics
Fundamental and applied biological sciences. Psychology
Gamma Rays
Liver - drug effects
Liver - metabolism
Liver - radiation effects
Male
mdr1b gene
Mice
Mice, Knockout
Molecular and cellular biology
Molecular Sequence Data
Promoter Regions, Genetic
Radiation, Ionizing
Rats
Sequence Homology, Nucleic Acid
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Up-Regulation
Whole-Body Irradiation
title Mdr1b facilitates p53-mediated cell death and p53 is required for Mdr1b upregulation in vivo
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