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BCL2 — CD40

Text-mined interactions from Literome

Fujieda et al., Oncol Res 1998 (Carcinoma...) : CD40 stimulation enhanced Bcl-2 expression, and antisense oligonucleotide against bcl-2 canceled the inhibition of HTC/C3 cell growth caused by CD40 stimulation
Taylor et al., Endocr Relat Cancer 1999 (Lymphoma, B-Cell...) : CD40 receptor ligation resulted in increased levels of Bcl-XL
An et al., Int J Oncol 2003 (Burkitt Lymphoma) : Anti-IgM triggers for cleavage of the resident nuclear proteins poly ( ADP-ribose ) polymerase ( PARP ) at 8 h, lamins B1 and B2 from 12 to 16 h ; likewise, ionomycin triggers for degradation of PARP at 2 h, lamins B1 and B2 at 4 h. Signal transduction through CD40 rescues Ramos-BL B cells from AgR- and ionomycin triggered apoptosis at a very early stage of the apoptotic process by inhibiting both the early cleavage of PARP as well as the activation of caspase-3, -7 and -8 and cleavage of lamin B1 ; CD40 mediated rescue occurs upstream of CD40 induced expression of Bcl-2 and increased expression of Bcl-xL
Hirai et al., Cell Death Differ 2004 : Expression of Bcl-xL and A1, antiapoptotic members of the Bcl-2 family, is enhanced by CD40 ligation, and is suggested to mediate CD40 induced B-cell survival
Ke et al., Mol Ther 2004 (Liver Diseases...) : Ad-CD40Ig reduced frequency of TUNEL+ cells and pro-apoptotic Caspase-3, but enhanced antioxidant HO-1 and anti-apoptotic Bcl-2/Bcl-xl expression
Zhou et al., Apoptosis 2005 (Lymphoma, B-Cell...) : CD40 activation stimulated both anti-apoptotic Bcl-XL and pro-apoptotic Bax mRNA synthesis in the Daudi cell line ; CD40 activation increased the Bax mRNA level but had no effect on the Bcl-XL mRNA level in the XG2 cell line
Huang et al., Med Oncol 2011 (Uterine Cervical Neoplasms) : Furthermore, CD40 activation blocked SiHa in the S phase, stimulated proapoptotic Bax and inhibited antiapoptotic Bcl-XL mRNA synthesis in the SiHa cell
Ishida et al., J Immunol 1995 : CD40 signaling mediated induction of Bcl-XL , Cdk4, and Cdk6
Zhang et al., Mol Cell Biol 1994 (Leukemia, Lymphocytic, Chronic, B-Cell...) : In contrast to I kappa B alpha ( MAD3 ), BCL3 does not cause NF-kappa B p50 to be retained in the cytoplasm ; instead, in cotransfection assays, it alters the subnuclear localization of p50
Eliopoulos et al., Oncogene 1996 (Urinary Bladder Neoplasms) : The expression of Bcl-2 did not affect growth inhibition induced by CD40 ligation in epithelial cells but the Epstein - Barr Virus encoded latent membrane protein 1 (LMP1) blocked the effect
Fang et al., Am J Physiol 1997 : CD40 signaling led to a rapid increase in the expression of the apoptosis inhibitory protein Bcl-xL
An et al., Cell Immunol 1997 (Burkitt Lymphoma) : This CD40 potentiated Fas triggered growth inhibition and apoptosis occurs in the presence of CD40 induced expression of the anti-apoptotic proteins Bcl-xL and Bcl-2
Curnock et al., Cell Immunol 1998 (Burkitt Lymphoma) : The LY-mediated induction of growth inhibition and apoptosis occurs in the presence of the CD40 induced anti-apoptotic protein Bcl-XL ... Taken together these data indicate that the CD40 of Ramos BL B cells is linked to PI3-kinase independent and -dependent routes of survival : CD40 mediated inhibition of AgR triggered caspase-3-like activity, PARP cleavage, and CD40 triggered Bcl-XL expression are PI3-kinase independent, whereas PI3-kinase is critical for CD40 mediated rescue of this cellular population from AgR triggered growth inhibition, caspase-3 processing, and apoptosis