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BCL2 — BCL6

Text-mined interactions from Literome

Roberts et al., J Immunol 1999 : We show that B cell Ag receptor signaling in the absence of coreceptor recruitment induces cellular accumulation of the anti-apoptotic protein Bcl-xL , whereas CD19 mediated signals are required for Bcl-2 accumulation
Elliott et al., Cancer Chemother Pharmacol 1999 (Cell Transformation, Neoplastic) : In addition, Bcl-2 also prevented the increase in cellular levels of Bak, Bax and Bcl-xL , along with degradation of actin and Bax
Tagami et al., Oncogene 2000 (Translocation, Genetic) : RTN-XS interacted with both Bcl-XL and Bcl-2 , increased the localization of Bcl-XL and Bcl-2 on the ER, and reduced the anti-apoptotic activity of Bcl-XL and Bcl-2
Mihara et al., Int J Oncol 2002 (Carcinoma, Squamous Cell...) : We also found up-regulation of Bcl-xS in the former cell lines, and in the latter cell lines, the expressions of Bcl-2 and Bcl-xL were induced simultaneously
Tung et al., Am J Physiol Heart Circ Physiol 2003 : These changes in the Fas-Fas ligand pathway and Bcl-2 mitochondrial apoptosis regulation are enhanced by complete suppression of antiapoptotic FADD-like IL-1beta converting enzyme inhibitory protein ( FLIP ) ( from 30.5 to 0.0 %, P < 0.01 ) and Bcl-xL ( from 22.5 to 0.1 %, P = 0.03 ) expression among these cells from the earliest days after gene transfer
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
Saito et al., Proc Natl Acad Sci U S A 2009 (Lymphoma, Large B-Cell, Diffuse...) : BCL6 binds to the BCL2 promoter region by interacting with the transcriptional activator Miz1 and suppresses Miz1 induced activation of BCL2 expression ... BCL6 mediated suppression of BCL2 is lost in FL and DLBCL, where the 2 proteins are pathologically coexpressed, because of BCL2 chromosomal translocations and other mechanisms, including Miz1 deregulation and somatic mutations in the BCL2 promoter region
Zeng et al., J Ethnopharmacol 2010 : Moreover, MWG extract decreased the level of intracellular reactive oxygen species ( ROS ), increased MMP, regulated Bcl-2 family protein expression ( Bcl-2 and Bcl-XL ) and inhibited the release of cytochrome c from the mitochondria
Hu et al., Gut 2011 (Disease Models, Animal...) : It was shown that arginine induced expression of Bcl-2 and Bcl-xL , while rReg4 upregulated Bcl-2 and Bcl-xL expression by activating the EGFR/Akt pathway
Erdman et al., Adv Gerontol 2012 : In female of longevity age, the number of CASP8*I/*D, BCL2*T/*T and BAX*A/*A genotype carriers was higher and number of CASP8*DI/*D, BCL2*C/*C , BAX*A/*G and BAX *G/*G genotype carriers was reduced
Whitehead et al., J Perinatol 2013 (Fetal Growth Retardation...) : In preterm PE, but not FGR, there was increased placental expression of BCL-XL and BCL2 ( 1.6 to 2.5-fold, P < 0.05 ), but only BCL2 was significantly increased in the maternal blood ( 1.8-fold, P < 0.05 )
Tripathi et al., Cell Death Differ 2013 : Although Bcl-2 is an important Bim antagonist in effector T cells, and Bcl-xL is not required for effector T-cell survival, the roles of other anti-apoptotic Bcl-2 family members remain unclear
Greenlund et al., Neuron 1995 : Therefore, BCL-2 is an important regulator of the survival of sympathetic neurons after NGF deprivation during the period of naturally occurring programmed neuronal death, but BCL-2 is not involved in the development of trophic factor independence in mature sympathetic neurons
Sumantran et al., Cancer Res 1995 (Breast Neoplasms) : We used Bcl-XS , a dominant negative inhibitor of Bcl-2 and Bcl-XL, to demonstrate the role of these genes in modulating chemotherapy induced apoptosis
Woolveridge et al., Mol Hum Reprod 1998 (Prostatic Neoplasms) : However, in the long-term treated testes, Bcl-xl and PARP expression declined, Bax and p53 protein concentrations were unchanged, and Bcl-2 was up-regulated
Tao et al., J Biol Chem 1998 : Bcl-xS and Bad potentiate the death suppressing activities of Bcl-xL, Bcl-2 , and A1 in yeast