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BCL3 — JUN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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IRef Biogrid Interaction:
BCL3
—
JUN
(physical association, affinity chromatography technology)
Na et al., J Biol Chem 1999*
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IRef Biogrid Interaction:
BCL3
—
JUN
(direct interaction, pull down)
Na et al., J Biol Chem 1999*
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IRef Biogrid Interaction:
BCL3
—
JUN
(direct interaction, two hybrid)
Na et al., J Biol Chem 1999*
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IRef Hprd Interaction:
BCL3
—
JUN
(in vivo)
Na et al., J Biol Chem 1999*
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IRef Hprd Interaction:
BCL3
—
JUN
(in vitro)
Na et al., J Biol Chem 1999*
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IRef Ophid Interaction:
BCL3
—
JUN
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Rebollo et al., Mol Cell Biol 2000
:
Overexpression of
Jun family proteins transactivates the promoter and
restores Bcl-3 expression in the absence of IL-4 stimulation
Yao et al., J Neurosci 2007
:
In the presence of toxic levels of Abeta, we observe that E2 attenuates indices of neuronal apoptosis :
c-Jun N-terminal kinase (JNK) dependent downregulation of
Bcl-w and upregulation of Bim, mitochondrial release of cytochrome c and Smac, and cell death
Jeong et al., Biol Pharm Bull 2008
(Brain Neoplasms...) :
Here, we confirmed that stable expression of
B-cell lymphoma-xL ( Bcl-xL ) in N18TG neuroglioma cells could
suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment
Jacobs-Helber et al., Mol Cell Biol 1998
:
A dominant negative
AP1 mutant rendered these cells resistant to apoptosis induced by EPO withdrawal and
blocked the downregulation of
Bcl-XL