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BCL3 — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Vitale et al., Endocrinology 2000
(Necrosis) :
This type of apoptosis is
p53 independent, does not require protein synthesis, and is not
induced by modulation of Bcl-2,
Bcl-XL , or Bax protein expression
Takehara et al., Hepatology 2001
(Carcinoma, Hepatocellular...) :
Ectopic expression of transcriptionally active
p53 alone was not sufficient for the activation of apoptosis in p53-null Hep3B cells, but apoptosis was
induced when endogenous
Bcl-xL was simultaneously inhibited by antisense oligonucleotide in these cells
Rocha et al., Mol Cell Biol 2003
:
p53 inhibited the expression of Bcl-3 protein, a member of the IkappaB family that functions as a transcriptional coactivator for p52 NF-kappaB and also
reduced p52/Bcl-3 complex levels
Raymond et al., FASEB J 2004
:
VSMC exposed to serum-free medium conditioned by apoptotic EC showed increased ERK 1/2 phosphorylation, enhanced
Bcl-xl expression, and
inhibition of
p53 expression
Kashatus et al., Genes Dev 2006
:
Experiments presented here indicate that
Bcl-3 is inducible by DNA damage and is
required for the induction of Hdm2 gene expression and the suppression of persistent
p53 activity
Sirach et al., Cell Death Differ 2007
(Carcinoma, Hepatocellular...) :
Finally, KLF6 silencing caused
p53 upregulation and
inhibited Bcl-xL expression, to induce cell death by apoptosis
Lee et al., Int J Cancer 2008
(Carcinoma, Squamous Cell...) :
Greater modulation among HNSCC lines expressing low wt p53 than those over expressing mt p53 protein suggested that decreased
p53 expression might
enhance activation of NF-kappaB, STAT3 and
BCL-XL
Ranuncolo et al., J Biol Chem 2008
:
Although BCL6 can directly repress
TP53 in centroblasts,
BCL6 induced TP53 expression in primary fibroblasts and B-cells, and these cells underwent p53 dependent growth arrest and senescence in the presence of physiological levels of BCL6
Zhou et al., Cell Mol Immunol 2009
:
Treatment of CpG DNA could reduce the expression of caspase 3, increase IAP and
Bcl-xL expressions, and
inhibit p53 protein expression which level was increased in B cell spontaneous apoptosis at 24 h. AKT kinase activity was increased with the incubation of CpG DNA
Lee et al., Chem Biol Interact 2011
:
TRAIL induced nuclear damage, decreased Bid, Bcl-2,
Bcl-xL and survivin protein levels,
increased Bax levels, induced cytochrome c release, activated caspases ( -8, -9 and -3 ) and increased
tumor suppressor p53 levels
Banu et al., Toxicol Appl Pharmacol 2011
:
Our data indicated that CrVI : ( i ) induced DNA fragmentation and increased apoptosis, ( ii ) increased cytochrome c release from the mitochondria to cytosol, ( iii ) downregulated anti-apoptotic Bcl-2,
Bcl-XL , HSP70 and HSP90 ; upregulated pro-apoptotic BAX and BAD, ( iv ) altered translocation of Bcl-2, Bcl-XL, BAX, BAD, HSP70 and HSP90 to the mitochondria, ( v ) upregulated p-ERK and p-JNK, and selectively translocated p-ERK to the mitochondria and nucleus, ( vi ) activated caspase-3 and PARP, and ( vii ) increased phosphorylation of
p53 at ser-6, ser-9, ser-15, ser-20, ser-37, ser-46 and ser-392,
increased p53 transcriptional activation, and downregulated MDM-2
Park et al., Mol Carcinog 2012
(Colonic Neoplasms...) :
HFD feeding increased tumor tissue levels of Ki67, cyclin A, cyclin D1, CDK2,
Bcl-xL , and Bcl-2 ; reduced
p53 levels and TUNEL positive apoptotic cells ;
increased the levels of CD45, CD68, CD31, VEGF, P-VEGF receptor-2, iNOS, and COX-2 as well as hemoglobin content ; and increased the levels of HIF-1a, P-STAT3-Y705, P-STAT3-S727, P-I?B-a, P-p65, p65, P-c-Jun, P-Akt, P-ERK1/2, P-p38, and P-SAPK/JNK
Li et al., Dalton Trans 2012
(Neoplasms) :
DNA damage subsequently activated
p53 phosphorylation and
inhibited the expression of
Bcl-xL , resulting in activation of caspase-3, -8 and -9, and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Merchant et al., Oncogene 1996
:
These observations indicate that Bcl-2 and
Bcl-xL are regulated differently in
response to wild-type
p53 activity and that, while correction of mutant p53 phenotype may effectively kill cells having Bcl-2 as their major defense against PCD, this is not necessarily the case in cells using Bcl-xL as their primary defense