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ABCB1 — TP53
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Nicoletti et al., Int J Oncol 2001
(Kidney Neoplasms) :
Wt
p53 mediated
induction of endogenous
MDR-1 may represent a rudiment of cellular protection against toxic compounds earlier in evolution
Lecureur et al., Oncogene 2001
:
Mdr1b facilitates p53 mediated cell death and
p53 is
required for Mdr1b upregulation in vivo
Ros et al., Hepatology 2001
(Carcinoma, Hepatocellular...) :
Induction of
Mdr1b expression by tumor necrosis factor-alpha in rat liver cells is
independent of
p53 but requires NF-kappaB signaling ... Because p53 is up-regulated by TNF-alpha in an NF-kappaB dependent manner and the Mdr1b promoter contains a p53 binding site, we used liver cells expressing a dominant negative p53 to show that TNF-alpha up-regulation of
Mdr1b is
independent of functional
p53
Bush et al., Carcinogenesis 2002
:
The general model proposes that wild-type p53 down regulates, while mutant
p53 up
regulates , the
Mdr1 promoter
Chin et al., Science 1992
:
The stimulatory effect of c-Ha-Ras-1 was not specific for the MDR1 promoter alone, whereas a mutant
p53 specifically
stimulated the
MDR1 promoter and wild-type p53 exerted specific repression
Vilgelm et al., Oncogene 2008
(Carcinoma...) :
Our data suggest that upregulation of
MDR1 by DeltaNp73alpha is
mediated by interaction with
p53 at the MDR1 promoter
He et al., Zhonghua Yi Xue Za Zhi 2007
(Breast Neoplasms) :
Ad-p53 can
inhibit the expression of
MDR1 gene and partially reverse the MDR of MCF-7/ADM cells, thus enhancing the chemosensitivity of human breast cancer cells to ADM
Nardinocchi et al., PloS one 2009
:
Zinc supplementation to hypoxia treated cells increased HIPK2 protein stability and nuclear accumulation, leading to restoration of HIPK2 binding to HIF-1alpha promoter, repression of
MDR1 , Bcl2, and VEGF genes, and
activation of the
p53 apoptotic response to drug
Chuang et al., Toxicol In Vitro 2012
(Neoplasms) :
We demonstrated that
p53 is
induced by low dose DOC treatment, resulting in
MDR-1 gene suppression in human lung cancer cells
Lin et al., Oncogene 1995
(Neoplasms, Experimental) :
Some mutant forms of the p53 protein have been shown to gain new functions that are not shared by the wild-type p53 protein ; ( 1 ) mutant p53 proteins can transcriptionally transactivate the
multi-drug resistance gene-1 (MDR-1) and ( 2 ) when expressed in non-tumorigenic cells with no endogenous p53 protein, mutant
p53 proteins can
enhance the tumorigenic potential of these cells ( Dittmer et al., 1993 )
Schneider et al., J Natl Cancer Inst 1994
(Breast Neoplasms...) :
Recently, it has been demonstrated that in vitro both c-Ha-Ras overexpression and mutant
p53 overexpression do
activate the
MDR1 gene ( also known as PGY1 ) in murine NIH 3T3 cells
Nguyen et al., Oncol Res 1994
:
To further characterize the
effects of
p53 on the
MDR1 promoter, we have shown in the current study that the region of the promoter that is required for transactivation by p53 mutants overlaps with the region that is essential for basal promoter activity ... In addition, we also have shown that several different
p53 mutants
transactivate the
MDR1 promoter in several different cell types, including embryo fibroblasts derived from the p53-deficient ( p53-l- ) mice generated by gene targeting
el Rouby et al., Blood 1993
(Leukemia, Lymphocytic, Chronic, B-Cell) :
In addition to examining the clinical relevance of p53 gene mutations in B-CLL, we investigated the possible
role of
p53 gene regulation in the expression of the multidrug resistance genes
MDR1 and MDR3
de Kant et al., J Cancer Res Clin Oncol 1996
(Colorectal Neoplasms...) :
As a transcriptional regulator,
p53 might be
involved in regulation of
MDR1 expression in these tumours ... These data indicate that mutant
p53 may
play a role in the regulation of
MDR1 expression in human cholorectal cancer
Thottassery et al., Proc Natl Acad Sci U S A 1997
(Carcinoma, Hepatocellular...) :
p53 dependent regulation of
MDR1 gene expression causes selective resistance to chemotherapeutic agents