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BCL3 — TNF

Text-mined interactions from Literome

Heissmeyer et al., EMBO J 1999 : TNF-alpha induced Bcl-3-p50 formation requires proteasome activity, but is independent of p50-p65 released from IkappaBalpha, indicating a pathway that involves p105 proteolysis
Brasier et al., J Biol Chem 2001 : Two observations are interpreted to indicate that bcl-3 is transactivated by NF-kappa B/Rel A : 1 ) expression of a dominant negative NF-kappa B inhibitor blocks tumor necrosis factor-alpha induced BCL-3 expression and 2 ) expression of constitutively active Rel A is sufficient to induce BCL-3 expression
Soeda et al., Life Sci 2001 : Moreover, crocin suppressed the TNF-alpha induced expression of Bcl-Xs and LICE mRNAs and simultaneously restored the cytokine induced reduction of Bcl-X ( L ) mRNA expression
Kuwata et al., Blood 2003 : IL-10-inducible Bcl-3 negatively regulates LPS induced TNF-alpha production in macrophages ... Lentiviral vector mediated expression of Bcl-3 inhibited lipopolysaccharide (LPS) induced production of tumor necrosis factor alpha (TNF-alpha) , but not IL-6, in macrophages ... Overexpression of Bcl-3 suppressed activation of the TNF-alpha promoter, but not the IL-6 promoter ... These findings suggest that IL-10 induced Bcl-3 is required for suppression of TNF-alpha production in macrophages
Wessells et al., J Biol Chem 2004 : Forced expression of BCL-3 suppressed LPS induced transcription from the TNFalpha promoter and inhibited two artificial promoters composed of TNFalphakappaB sites that preferentially bind p50 dimers ... Analysis of macrophages from p50 and BCL-3 knock-out mice revealed that both transcription factors negatively regulate TNFalpha expression and that BCL-3 inhibits IL-1alpha and IL-1beta
Yang et al., Zhonghua Gan Zang Bing Za Zhi 2005 : [ Bcl-xl blocks tumor necrosis factor alpha induced caspase 8 activation and apoptosis ]
Cassatella et al., Eur J Immunol 2005 : In this study, we show that modulation by IL-10 of LPS induced TNF-alpha , CXCL8/IL-8 and IL-1 receptor antagonist (IL-1ra) mRNA accumulation in neutrophils already expressing a functional IL-10R and antigenic SOCS-3 ( i.e. in `` 4-h cultured '' neutrophils ) occurs with kinetics that are similar to those observed in `` time 0 '' neutrophils, depends on de novo protein synthesis, but does not require SOCS-1, SOCS-3, heme oxygenase and Bcl-3 induction
Zhang et al., Arthritis Rheum 2005 (Arthritis, Experimental...) : Bcl-xL or Ets-2 overexpression protected osteoclasts from ALN induced apoptosis, and TNF stimulated Bcl-xL and Ets-2 expression in osteoclasts
Wang et al., Clin Cancer Res 2005 (Breast Neoplasms...) : Further investigation showed that silencing of hPEBP4 in MCF-7 cells promoted TNF-alpha induced stability of p53, up-regulation of phospho-p53ser15, p21waf/cip, and Bax, and down-regulation of Bcl-2 and Bcl-xL , which were shown to depend on extracellular signal regulated kinase 1/2 and c-jun NH2-terminal kinase activation by hPEBP4 silencing
Zhang et al., Endocrinology 2007 : These data suggest that in wild-type MEC, TNF stimulates the interaction of bcl3 with p50 and p52, and the binding of p52, as well as RelB, to cyclin D1 promoter kappaB sites, and as a consequence, stimulates the growth of MEC
Dhingra et al., Am J Physiol Heart Circ Physiol 2007 : The antioxidant Trolox modulated TNF-alpha induced changes in Bax/Bcl-xl , cell injury, and MAPKs
Brenne et al., Eur J Haematol 2009 (Multiple Myeloma) : Bcl-3 was induced in myeloma cell lines by interleukin (IL)-6, IL-21, IL-15, tumor necrosis factor-alpha and IGF-1, and its upregulation was associated with increased proliferation of the cells
Bala et al., J Leukoc Biol 2012 : In summary, our novel data suggest that acute alcohol treatment in vitro and in vivo induces molecular signatures of TLR4/LPS tolerance through the induction of Bcl-3 , a negative regulator of TNF-a transcription via its association with NF-?B p50/p50 dimers
Slowik et al., Lab Invest 1997 : TNF + CHX killing is effectively blocked by transfected CrmA protein or treatment with Z-VAD.fmk peptide-both inhibitors of interleukin-1 converting enzyme-like proteases-but not by transfected antiapoptotic proteins Bcl-2, Bcl-XL , or A1 ... TNF + cer killing, which can affect more than 50 % of EC, is not effectively inhibited by CrmA or Z-VAD frank, but can be readily blocked by Bcl-2, Bcl-XL , or A1