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BCL2 — TGFB1

Text-mined interactions from Literome

Francis et al., J Biol Chem 2000 : Transforming growth factor-beta 1 induces apoptosis independently of p53 and selectively reduces expression of Bcl-2 in multipotent hematopoietic cells
Katayama et al., Leukemia & lymphoma 2000 : The effects of TGF-beta1 on Bcl-2 and p27 expression as well as cell growth were abrogated by c-kit ligand
Negulescu et al., Kidney Int 2002 : The effects of TGF-beta1 on mesangial cell apoptosis, p53 phosphorylation, Bax and Bcl-2 levels, caspase 9 activity, and cleavage of PARP were examined
Chatzaki et al., Mol Hum Reprod 2003 : We have found the following : ( i ) TGFbeta1 induced apoptosis of stromal cells in a time- and dose dependent manner ; ( ii ) blockade of TGFbeta1 's autocrine/paracrine effect by TGFbeta1 neutralizing antibodies diminished the basal rate of stromal cell apoptosis ; ( iii ) semi-quantitative Western blot analysis showed that TGFbeta1 caused a rapid but transient elevation of the pro-apoptotic FasL protein, without affecting the levels of Fas receptor ; ( iv ) TGFbeta1 increased the levels of the anti-apoptotic Bcl-2 and Bcl-xL proteins, while having no significant effects on the pro-apoptotic proteins Bax and Bak, suggesting the activation of a transient survival mechanism activated in stromal cells as a parallel rescue response to the apoptosis inducing FasL protein
von Willebrand et al., Exp Dermatol 2005 (Melanoma...) : FGF-2 blocks TGF-beta1 mediated suppression of Bcl-2 in normal melanocytes ... Instead, TGF-beta1 decreased the level of Bcl-2 in normal melanocytes cultured on collagen gel, and FGF-2 reversed the TGF-beta1 mediated reduction in the level of Bcl-2 ... In nevus and melanoma cells, TGF-beta1 was unable to induce a decrease in the level of Bcl-2 , and treatment with FGF-2 did not cause an increase in the level of Bcl-2 in nevus or melanoma cells
Wada et al., Kidney Int 2005 : TGF-beta1 increased the protein levels of an anti-apoptotic Bcl-2 in p21-/- podocytes, but not in p21+/+ podocytes ... Moreover, TGF-beta1 did not increase Bcl-2 expression in p21-/- podocytes in which p21 expression was restored
Lu et al., Am J Physiol Lung Cell Mol Physiol 2008 (Emphysema) : In addition, the baseline level of Bcl-2 was enhanced by TGF-beta1 and reduced by inhibition of activin receptor-like kinase 5 (ALK5), a TGF-beta1 type I receptor
Li et al., Neurotox Res 2010 (Anoxia) : Astrocytes beta ( 8 ) could induce TGF-beta1 leading to upregulation of Bcl-2 and Bcl-xL , and thus attenuated neuronal apoptosis
Yu et al., Zhongguo Shi Yan Xue Ye Xue Za Zhi 2010 : The TGF-beta1 ( 5 ng/ml ) induced arrest of cells in G1 phase ( p < 0.05 ) compared with As2O3 alone and As2O3 combined with TGF-ß1, while there was no difference with control. P27 ( Kip1 ) expression was up regulated ( p < 0.05 ), cyclin E and BCL-2 expression was down-regulated ( p < 0.05 ) in TGFß1 treated group. BCl-2 expression was down regulated, endogenesis TGFß1 expression was up regulated ( p < 0.05 ), and the level of P27 ( kip1 ) and cyclin E were not changed in As2O3 treated group ( p > 0.05 )
Selvakumaran et al., Oncogene 1994 (Leukemia, Myeloid, Acute) : Both p53 and TGF beta 1 down-regulated endogenous Bcl-2 expression, but only p53 up-regulated Bax expression, where bax has been identified as a p53 immediate early response gene
Roth et al., Semin Oncol 1996 (Neoplasms, Hormone-Dependent...) : BCL2 expression is increased in androgen independent cells, which may block apoptosis, and retinoids induce transforming growth factor-beta and apoptosis in prostate cancer cell lines