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BCL6 — JUN
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Vasanwala et al., J Immunol 2002
(Cell Transformation, Neoplastic) :
An estrogen receptor ligand binding domain fusion with the BCL-6 zinc finger domain can act as a estrogen-inducible dominant negative protein and increase AP-1 activity in BCL-6 ( + ) cells but not in BCL-6 ( - ) cells, indicating that endogenous
BCL-6 represses
AP-1 activity
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