Induction of <i>bcl</i>-2 Expression by Phosphorylated CREB Proteins during B-Cell Activation and Rescue from Apoptosis

Wilson, Byron E.; Mochon, Evonne; Boxer, Linda M.

doi:10.1128/mcb.16.10.5546

Cited by 396 publications

(352 citation statements)

References 59 publications

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“…A significant increase in pCREB was noted 4 h after xenon exposure ( Figure 6A); conversely, N 2 O exposure, which does not precondition, did not induce pCREB ( Figure 6B). Phosphorylation of CREB at serine 133 allows CREB to recruit coactivators such as CREB-binding protein (CBP) and RNA polymerase II to activate transcription of CREB-dependent genes including the prosurvival protein, Bcl-2 (Wilson et al, 1996), and BDNF (Tao et al, 1998). Bcl-2 and BDNF were significantly upregulated 4 h after xenon treatment ( Figure 6C).…”

Section: Effect On Long-term Neurologic Functionmentioning

confidence: 99%

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

Hossain

Pettet

et al. 2006

J Cereb Blood Flow Metab

166

111

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Xenon attenuates on-going neuronal injury in both in vitro and in vivo models of hypoxic-ischaemic injury when administered during and after the insult. In the present study, we sought to investigate whether the neuroprotective efficacy of xenon can be observed when administered before an insult, referred to as 'preconditioning'. In a neuronal-glial cell coculture, preexposure to xenon for 2 h caused a concentration-dependent reduction of lactate dehydrogenase release from cells deprived of oxygen and glucose 24 h later; xenon's preconditioning effect was abolished by cycloheximide, a protein synthesis inhibitor. Preconditioning with xenon decreased propidium iodide staining in a hippocampal slice culture model subjected to oxygen and glucose deprivation. In an in vivo model of neonatal asphyxia involving hypoxic-ischaemic injury to 7-day-old rats, preconditioning with xenon reduced infarction size when assessed 7 days after injury. Furthermore, a sustained improvement in neurologic function was also evident 30 days after injury. Phosphorylated cAMP (cyclic adenosine 3 0 ,5 0 -monophosphate)-response element binding protein (pCREB) was increased by xenon exposure. Also, the prosurvival proteins Bcl-2 and brain-derived neurotrophic factor were upregulated by xenon treatment. These studies provide evidence for xenon's preconditioning effect, which might be caused by a pCREB-regulated synthesis of proteins that promote survival against neuronal injury.

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Section: Effect On Long-term Neurologic Functionmentioning

confidence: 99%

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

Hossain

Pettet

et al. 2006

J Cereb Blood Flow Metab

166

111

View full text Add to dashboard Cite

show abstract

“…Activation of CREB by Akt phosphorylation triggers recruitment of the coactivator CREB-binding protein (CBP) 49 and promotes transcription of specific prosurvival genes such as BCL-2. 50 The NF-kB transcription factor promotes cell survival in response to several apoptotic stimuli. Phosphorylation and activation of its positive regulator IkB kinase by Akt leads to phosphorylation and degradation of IkB, an inhibitor of NF-kB, promoting nuclear translocation of NF-kB and activation of its target genes.…”

Section: The Role Of Akt In Signal Transductionmentioning

confidence: 99%

The emerging role of the PI3-K-Akt pathway in prostate cancer progression

Ittmann

Ayala

et al. 2005

Prostate Cancer Prostatic Dis

112

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The PI3-K-Akt pathway plays a central role in the development and progression of prostate cancer and other malignancies. We review original studies and summarize relevant sections of previous reviews concerning the relationships between abnormalities in the PI3-K-Akt pathway and prostate cancer progression. We discuss laboratory and clinical data that indicate gene perturbation and dysregulation of PI3-K-Akt pathway is common in prostate cancer and other malignancies. We further discuss the critical role of the PI3-K-Akt pathway in the oncogenic signaling network and provide examples that establish the PI3-K-Akt pathway as a focal point for the future development of informative biomarkers and effective therapies for prostate cancer.

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“…Given its fundamental importance for cellular fate, BCL2 expression is finely tuned by a variety of environmental and endogenous stimuli and regulated at both transcriptional and posttranscriptional levels (Young and Korsmeyer, 1993;Miyashita et al, 1994;Heckman et al, 2000;Schiavone et al, 2000;Wu et al, 2001;Heckman et al, 2002;Donnini et al, 2004). At the transcriptional level the expression of the BCL2 gene is regulated by both positive and negative elements located within both the promoter and coding regions (Chen and Boxer, 1995;Wilson et al, 1996;Perillo et al, 2000;Lang et al, 2005). Our previous investigations demonstrated that the BCL2 major breakpoint region (mbr) in the 3 0 -UTR upregulates reporter gene expression, which implies that this region possessed intrinsic regulatory function (Zhang et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The BCL2 major breakpoint region (mbr) regulates gene expression

Zhang

Durrin

et al. 2006

Oncogene

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BCL2 expression is finely tuned by a variety of environmental and endogenous stimuli and regulated at both transcriptional and post-transcriptional levels. Our previous investigations demonstrated that the BCL2 major breakpoint region (mbr) in the 3 0 -UTR upregulates reporter gene expression, which implies that this region possessed intrinsic regulatory function. However, the effect of the mbr on BCL2 expression, and the underlying regulatory mechanisms, remain to be elucidated. To assess the direct effect of the mbr on the transcriptional activity of the BCL2 gene, we employed targeted homologous recombination to establish a mbr þ /mbr À heterozygous Nalm-6 cell line and then compared the transcriptional activity and apoptotic effect on transcription between the wild type and targeted alleles. We found that deletion of the mbr significantly decreased the transcriptional activity of the corresponding allele in the mbr þ /mbr À cell. The BCL2 allele deleted of the mbr had a slower response to apoptotic stimuli than did the wild type allele. The regulatory function of the mbr was mediated through SATB1. Overexpression of SATB1 increased BCL2 expression, while knockdown of SATB1 with RNAi decreased BCL2 expression. Our results clearly indicated that the mbr could positively regulate BCL2 gene expression and this regulatory function was closely related to SATB1.

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Induction of bcl-2 Expression by Phosphorylated CREB Proteins during B-Cell Activation and Rescue from Apoptosis

Cited by 396 publications

References 59 publications

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

The emerging role of the PI3-K-Akt pathway in prostate cancer progression

The BCL2 major breakpoint region (mbr) regulates gene expression

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