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Akt/Protein Kinase B Up-regulates Bcl-2 Expression through cAMP-response Element-binding Protein*
Data indicate that regulation of Bcl-2 expression by IGF-I involves a signaling cascade mediated by PI 3-kinase/PDK1/Akt/CREB, and the observation that enhanced CREB activity by Akt signaling leads to increased B cl-2 promoter activity and cell survival.
Induction of bcl-2 expression by phosphorylated CREB proteins during B-cell activation and rescue from apoptosis
The CRE site in the bcl-2 promoter appears to play a major role in the induction of bCl-2 expression during the activation of mature B cells and during the rescue of immature B cells from apoptosis.
Translocations involving c-myc and c-myc function
Parts of c-myc gene activation and the function of the c-Myc protein are reviewed, suggesting that while c- myc is not required for cell proliferation, it acts as an integrator and accelerator of cellular metabolism and proliferation.
Negative regulation of bcl-2 expression by p53 in hematopoietic cells
The TATA sequence in the bcl-2 P2 minimal promoter is the target for repression by p53, and the interaction between p53 and TBP is most likely responsible for the repression.
p53 Suppresses the Activation of the Bcl-2 Promoter by the Brn-3a POU Family Transcription Factor*
- V. Budhram-Mahadeo, P. Morris, Martin D. Smith, C. Midgley, L. Boxer, D. Latchman
- Biology, ChemistryThe Journal of Biological Chemistry
- 21 May 1999
The Brn-3a POU family transcription factor has been shown to strongly activate expression of the Bcl-2proto-oncogene and thereby protect neuronal cells from programmed cell death (apoptosis) and the antagonistic effects of B cl-2 and p53 on the rate of apoptosis and the overexpression of Brn -3a in specific tumor cell types are discussed.
Oxidative stress‐mediated down‐regulation of bcl‐2 promoter in hippocampal neurons
It is demonstrated that loss of CREB function contributes to oxidative stress‐induced neuronal dysfunction.
Histone Deacetylase Inhibitors Down-Regulate bcl-2 Expression and Induce Apoptosis in t(14;18) Lymphomas
It is found that in addition to potent cell cycle arrest, TSA and NaB also dramatically induced apoptosis and down-regulated bcl-2 expression, and overexpression of b cl-2 inhibited TSA-induced apoptosis.
Insulin-like Growth Factor-I Induces bcl-2 Promoter through the Transcription Factor cAMP-Response Element-binding Protein*
A novel signaling pathway (MAPK kinase 6/p38β MAPK/MAPKAP-K3) is characterized that defines a transcriptional mechanism for the induction of the antiapoptotic protein Bcl-2 by IGF-I through the nuclear transcription factor cAMP-response element-binding protein in PC12 cells.
Transcription factor GATA4 regulates cardiac BCL2 gene expression in vitro and in vivo
- Satoru Kobayashi, Troy Lackey, Q. Liang
- BiologyFASEB journal : official publication of the…
- 1 April 2006
Results indicate that GATA4 positively regulates cardiac Bcl2 gene expression in vitro and in vivo.