◀ Back to TP53
BBC3 — TP53
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
BBC3
→
TP53
(increases, BBC3 Activity)
Evidence: NF?B family transcription factors can induce expression of antiapoptotic proteins that oppose the intrinsic (Bcl-XL, Bfl-1), extrinsic (FLIP), and convergence (cIAP2) pathways (Figure 2A), as well as suppressing expression of the death inducer Bax (intrinsic pathway) in some types of tumor cells (Karin and Lin, 2002). Further, hyperactivity of NF?B is now well documented in certain cancers (Karin et al., 2002).
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OpenBEL Selventa BEL large corpus:
BBC3
→
TP53
(increases, BBC3 Activity)
Evidence: These genes can be divided in three classes: one that controls cell-cycle arrest and senescence, one that controls apoptosis and one that regulates glucose metabolism and autophagy [42]. p53 is essentially known as a pro-apoptotic transcription factor that upregulates the expression of proteins such as BCL2-associated X protein (BAX), p53 upregulated modulator of apoptosis (PUMA) or NOXA.
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KEGG p53 signaling pathway:
BBC3
→
TP53
(gene expression, expression)
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NCI Pathway Database Direct p53 effectors:
PUMA/BCL2 subfamily complex (BBC3-BCL2_MCL1_BCL2L2_BCL2A1_BCL2L1)
→
p53 (TP53)
(modification, collaborate)
Chipuk et al., Science 2005
Evidence: mutant phenotype, physical interaction, other species
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NCI Pathway Database Direct p53 effectors:
PUMA/BCL2 subfamily complex (BBC3-BCL2_MCL1_BCL2L2_BCL2A1_BCL2L1)
→
p53/BCL2 subfamily complex (TP53-BCL2_MCL1_BCL2L2_BCL2A1_BCL2L1)
(modification, collaborate)
Chipuk et al., Science 2005
Evidence: mutant phenotype, physical interaction, other species
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NCI Pathway Database Direct p53 effectors:
p53 (TP53)
→
PUMA (BBC3)
(modification, collaborate)
Chipuk et al., Science 2005
Evidence: mutant phenotype, physical interaction, other species
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NCI Pathway Database Direct p53 effectors:
PUMA (BBC3)
→
p53/BCL2 subfamily complex (TP53-BCL2_MCL1_BCL2L2_BCL2A1_BCL2L1)
(modification, collaborate)
Chipuk et al., Science 2005
Evidence: mutant phenotype, physical interaction, other species
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WikiPathways TP53 Network:
TP53
→
Complex of PMAIP1-BBC3-BOK
(activation)
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WikiPathways Apoptosis:
TP53
→
PMAIP1/BBC3/BOK
(activation)
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WikiPathways miRNA Regulation of DNA Damage Response:
TP53
→
Complex of PMAIP1-BBC3-TP53AIP1-BAX
(activation)
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WikiPathways DNA Damage Response (only ATM dependent):
TP53
→
BBC3
(activation)
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WikiPathways DNA Damage Response:
TP53
→
Complex of PMAIP1-BBC3-TP53AIP1-BAX
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Kaeser et al., J Biol Chem 2004
(Colonic Neoplasms) :
Among a panel of p53 target genes tested by quantitative PCR, the gene showing the largest defect in induction by 5FU was
BBC3 ( PUMA ), which was
induced 4-fold by wild type
p53 and 2-fold by the N6A mutant
Li et al., J Biol Chem 2006
:
Endoplasmic reticulum stress induced apoptosis : multiple pathways and
activation of
p53-up regulated modulator of apoptosis ( PUMA ) and NOXA by
p53
Ghavami et al., PloS one 2011
:
Simvastatin concomitantly increased
p53 dependent expression of
p53 up-regulated modulator of apoptosis ( PUMA ), NOXA, and damage regulated autophagy modulator ( DRAM )
Bhattacharya et al., Invest Ophthalmol Vis Sci 2011
:
Activation of
p53 in response to Nutlin-3 also
increased levels of Noxa,
p53 upregulated modulator of apoptosis ( PUMA ), and Siva-1, decreased expression of Bcl-2 and Bcl-xL, and simultaneously increased caspases-9 and -3 activities and DNA fragmentation
Ghavami et al., Am J Physiol Lung Cell Mol Physiol 2012
:
Notably, GGT1 inhibition induced expression of
p53 dependent proteins,
p53 upregulated modulator of apoptosis ( Noxa ), and damage regulated autophagy modulator ( DRAM ), this was inhibited by the p53 transcriptional activation inhibitor cyclic-pifithrin-a