ArticleASN neuro2010
A single nucleotide polymorphism in the Bax gene promoter affects transcription and influences retinal ganglion cell death.
Article in ASN neuro, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Meta-analysis of transcriptomic changes in optic nerve injury and neurodegenerative models reveals a fundamental response to injury throughout the central nervous system.Molecular vision · 2017Pooled it
- Article
- The Role of microRNAs Related to Apoptosis forInternational journal of molecular sciences · 2024Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Increased Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.Investigative ophthalmology & visual science · 2021Article
- The basic science of optic nerve regeneration.Annals of translational medicine · 2021Review
- Too much death can kill you: inhibiting intrinsic apoptosis to treat disease.The EMBO journal · 2021Review
- Targeting HDAC3 in the DBA/2J spontaneous mouse model of glaucoma.Experimental eye research · 2020Article
- BAX-Depleted Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.Molecular neurobiology · 2020Article
- A broad perspective on the molecular regulation of retinal ganglion cell degeneration in glaucoma.Progress in brain research · 2020Review
- Completion of BAX recruitment correlates with mitochondrial fission during apoptosis.Scientific reports · 2019Article
- Axon injury signaling and compartmentalized injury response in glaucoma.Progress in retinal and eye research · 2019Review
- Targeting HDAC3 Activity with RGFP966 Protects Against Retinal Ganglion Cell Nuclear Atrophy and Apoptosis After Optic Nerve Injury.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2018Article
- AAV2-Mediated Transduction of the Mouse Retina After Optic Nerve Injury.Investigative ophthalmology & visual science · 2017Article
- Together JUN and DDIT3 (CHOP) control retinal ganglion cell death after axonal injury.Molecular neurodegeneration · 2017Article
- JUN is important for ocular hypertension-induced retinal ganglion cell degeneration.Cell death & disease · 2017Article
- BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.Progress in retinal and eye research · 2017Review
- Role of HDACs in optic nerve damage-induced nuclear atrophy of retinal ganglion cells.Neuroscience letters · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pro-apoptotic Bax is essential for RGC (retinal ganglion cell) death. Gene dosage experiments in mice, yielding a single wild-type Bax allele, indicated that genetic background was able to influence the cell death phenotype. DBA/2J(Bax+/-) mice exhibited complete resistance to nerve damage after 2 weeks (similar to Bax(-/-) mice), but 129B6(Bax+/-) mice exhibited significant cell loss (similar to wild-type mice). The different cell death phenotype was associated with the level of Bax expression, where 129B6 neurons had twice the level of endogenous Bax mRNA and protein as DBA/2J neurons. Sequence analysis of the Bax promoters between these strains revealed a single nucleotide polymorphism (T(129B6) to C(DBA/2J)) at position -515. A 1.5- to 2.5-fold increase in transcriptional activity was observed from the 129B6 promoter in transient transfection assays in a variety of cell types, including RGC5 cells derived from rat RGCs. Since this polymorphism occurred in a p53 half-site, we investigated the requirement of p53 for the differential transcriptional activity. Differential transcriptional activity from either 129B6 or DBA/2J Bax promoters were unaffected in p53(-/-) cells, and addition of exogenous p53 had no further effect on this difference, thus a role for p53 was excluded. Competitive electrophoretic mobility-shift assays identified two DNA-protein complexes that interacted with the polymorphic region. Those forming Complex 1 bound with higher affinity to the 129B6 polymorphic site, suggesting that these proteins probably comprised a transcriptional activator complex. These studies implicated quantitative expression of the Bax gene as playing a possible role in neuronal susceptibility to damaging stimuli.
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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.