◀ Back to BCL2

BCL2 — IL4

Text-mined interactions from Literome

Aronica et al., Cytokine 2000 : IL-4 dependent induction of BCL-2 and BCL-X ( L ) IN activated T lymphocytes through a STAT6- and pi 3-kinase independent pathway ... These results demonstrate that both the Stat6 and PI 3-kinase pathways can be dispensable for Bcl-2/X induction by IL-4 , thus suggesting the involvement of an additional signal transduction pathway
Graninger et al., Cell Death Differ 2000 (Lupus Erythematosus, Systemic) : IL-2, IL-4 , IL-7 and IL-15 led to a significant increase in Bcl-2 and a reduction in cell death rates, which was even more pronounced in SLE
Rebollo et al., J Immunol 2001 : IL-4 does not promote translocation of Aiolos or Bcl-xL , but induces tyrosine phosphorylation of Aiolos, which is required for dissociation from Bcl-xL
Wurster et al., J Biol Chem 2002 : We show that expression of the Bcl-2 family member, Bcl-xL , is induced maximally by IL-4 and anti-IgM/IL-4 in a Stat6 dependent manner
Dancescu et al., J Exp Med 1992 (Leukemia, Lymphocytic, Chronic, B-Cell) : Interleukin 4 protects chronic lymphocytic leukemic B cells from death by apoptosis and upregulates Bcl-2 expression
Rautajoki et al., Mol Cell Proteomics 2007 : We demonstrated that IL-4 decreases expression of Fas receptor and increases expression of Bid, Bcl-2, and Bcl-xL
Lin et al., Allergy 2007 (Dermatitis, Atopic) : Exogenously added IL-4 inhibited SEB induced caspase-3 activation and SEB induced decrease of Bcl-2 and Bcl-2 mRNA in SEB-reactive CD4+ T cells from healthy subjects ... Inhibition of endogenous IL-4 by using anti-IL-4 neutralizing antibodies up-regulated SEB induced caspase-3 activation and SEB induced decrease of Bcl-2 and Bcl-2 mRNA in SEB-reactive CD4+ T cells from AD patients
Burton et al., Mucosal Immunol 2013 : IL-4 induces Bcl-2 and Bcl-XL and enhances survival and stimulates proliferation in cultured bone marrow derived mast cells ( BMMC )
Gómez et al., Eur J Immunol 1997 : IL-2, but not IL-4 , induces Bcl-2 expression through RhoA activation which is inhibited by the specific Rho family inhibitor, Clostridium difficile Toxin B, as well as by a dominant negative RhoA mutant