ArticleMolecular neurodegeneration2011
BBC3 (PUMA) regulates developmental apoptosis but not axonal injury induced death in the retina.
Article in Molecular neurodegeneration, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
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- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Bax Contributes to Retinal Ganglion Cell Dendritic Degeneration During Glaucoma.Molecular neurobiology · 2022Article
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- Increased Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.Investigative ophthalmology & visual science · 2021Article
- Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins.Cell death and differentiation · 2021Review
- Endothelin 1-induced retinal ganglion cell death is largely mediated by JUN activation.Cell death & disease · 2020Article
- BAX-Depleted Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.Molecular neurobiology · 2020Article
- Axon injury signaling and compartmentalized injury response in glaucoma.Progress in retinal and eye research · 2019Review
- Mcl-1 and Bcl-xL are essential for survival of the developing nervous system.Cell death and differentiation · 2019Article
- Mkk4 and Mkk7 are important for retinal development and axonal injury-induced retinal ganglion cell death.Cell death & disease · 2018Article
- Role of SARM1 and DR6 in retinal ganglion cell axonal and somal degeneration following axonal injury.Experimental eye research · 2018Article
- Assessment of intrinsic and extrinsic signaling pathway in excitotoxic retinal ganglion cell death.Scientific reports · 2018Article
- 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
- Article
- BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.Progress in retinal and eye research · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNaturally occurring apoptosis is a developmental process that shapes the retina by eliminating overproduced neurons. In the absence of the proapoptotic Bcl-2 family member BAX, developmental apoptosis in the retina is disrupted and extra neurons survive. It is unknown how BAX is activated or if this regulation varies between neuronal types and subtypes. Since the Bcl-2 family members BIM, BID, and BBC3 (PUMA) are powerful direct activators of BAX, we used mice deficient for each of these genes to investigate their importance in developmental apoptosis.
resultsBax deficient mice have an increase in retinal ganglion cells (RGCs), bipolar cells and dopaminergic amacrine cells, but not photoreceptors, horizontal cells or cholinergic amacrine cells. The retinas of adult Bim and Bid deficient mice appeared to have no increase in any retinal cell type. Bbc3 deficient mice, either homozygous or heterozygous for a null allele of Bbc3, had an increase in the same cell types as Bax deficient mice. An analogous result may occur in the brain where, similar to Bax deficient mice, Bbc3 deficient mice have a larger gross brain weight compared to wild type mice. In contrast to its developmental role, BBC3 did not appear to be a primary factor in BAX-dependent axonal injury induced neurodegeneration in adult RGCs.
conclusionThe regulation of BAX activation in the retina appears to be complex, dependent on the developmental stage of the animal, the nature of the insult and even the type of neuron.
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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.