ArticleNucleic acids research2006
Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Linking metabolic dysfunction with cardiovascular diseases: Brn-3b/POU4F2 transcription factor in cardiometabolic tissues in health and disease.Cell death & disease · 2021Review
- The POU4F2/Brn-3b transcription factor is required for the hypertrophic response to angiotensin II in the heart.Cell death & disease · 2019Article
- Essential but partially redundant roles for POU4F1/Brn-3a and POU4F2/Brn-3b transcription factors in the developing heart.Cell death & disease · 2017Article
- Protein serine/threonine phosphatase PPEF-1 suppresses genotoxic stress response via dephosphorylation of PDCD5.Scientific reports · 2017Article
- Somatic Genomics and Clinical Features of Lung Adenocarcinoma: A Retrospective Study.PLoS medicine · 2016Article
- Co-expression of POU4F2/Brn-3b with p53 may be important for controlling expression of pro-apoptotic genes in cardiomyocytes following ischaemic/hypoxic insults.Cell death & disease · 2014Article
- Pou4f1 and pou4f2 are dispensable for the long-term survival of adult retinal ganglion cells in mice.PloS one · 2014Article
- ASPP1/2 regulate p53-dependent death of retinal ganglion cells through PUMA and Fas/CD95 activation in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
- Formation of stress-specific p53 binding patterns is influenced by chromatin but not by modulation of p53 binding affinity to response elements.Nucleic acids research · 2011Article
- Life or death: p53-induced apoptosis requires DNA binding cooperativity.Cell cycle (Georgetown, Tex.) · 2010Article
- Transcriptional regulation by p53.Cold Spring Harbor perspectives in biology · 2010Review
- The expanding universe of p53 targets.Nature reviews. Cancer · 2009Review
- Verification of genes differentially expressed in neuroblastoma tumours: a study of potential tumour suppressor genes.BMC medical genomics · 2009Article
- The non-apoptotic role of p53 in neuronal biology: enlightening the dark side of the moon.EMBO reports · 2009Review
- The p53 family and programmed cell death.Oncogene · 2008Review
- Cardiac expression of Brn-3a and Brn-3b POU transcription factors and regulation of Hsp27 gene expression.Cell stress & chaperones · 2008Article
- Characterization of genome-wide p53-binding sites upon stress response.Nucleic acids research · 2008Article
- Protein/DNA arrays identify nitric oxide-regulated cis-element and trans-factor activities some of which govern neuroblastoma cell viability.Nucleic acids research · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The Brn-3a and Brn-3b transcription factor have opposite and antagonistic effects in neuroblastoma cells since Brn-3a is associated with differentiation whilst Brn-3b enhances proliferation in these cells. In this study, we demonstrate that like Brn-3a, Brn-3b physically interacts with p53. However, whereas Brn-3a repressed p53 mediated Bax expression but cooperated with p53 to increase p21cip1/waf1, this study demonstrated that co-expression of Brn-3b with p53 increases trans-activation of Bax promoter but not p21cip1/waf1. Consequently co-expression of Brn-3b with p53 resulted in enhanced apoptosis, which is in contrast to the increased survival and differentiation, when Brn-3a is co-expressed with p53. For Brn-3b to cooperate with p53 on the Bax promoter, it requires binding sites that flank p53 sites on this promoter. Furthermore, neurons from Brn-3b knock-out (KO) mice were resistant to apoptosis and this correlated with reduced Bax expression upon induction of p53 in neurons lacking Brn-3b compared with controls. Thus, the ability of Brn-3b to interact with p53 and modulate Bax expression may demonstrate an important mechanism that helps to determine the fate of cells when p53 is induced.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.