ArticleMolecular and cellular neurosciences2012
BCL2L1 (BCL-X) promotes survival of adult and developing retinal ganglion cells.
Article in Molecular and cellular neurosciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Heat shock protein 40 enhances axon regeneration in a mouse model of traumatic optic neuropathy.Neural regeneration research · 2026Article
- Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Regulation of immunological equilibrium by IL-6/STAT3 in glaucomatous irises and its effect on filtering bleb success.Indian journal of ophthalmology · 2026Article
- Visual Neurorestoration: An Expert Review of Current Strategies for Restoring Vision in Humans.Brain sciences · 2025Review
- The Role of Endothelial Senescence in the Pathogenesis of Diabetic Retinopathy.International journal of molecular sciences · 2025Review
- 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
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- BclXCell death discovery · 2022Article
- Alternative splicing ofOncology letters · 2021Review
- Too much death can kill you: inhibiting intrinsic apoptosis to treat disease.The EMBO journal · 2021Review
- Antiapoptotic Bcl-2 family proteins BCL-xL and MCL-1 integrate neural progenitor survival and proliferation during postnatal cerebellar neurogenesis.Cell death and differentiation · 2021Article
- Proteome profiling of different rat brain regions reveals the modulatory effect of prolonged maternal separation on proteins involved in cell death-related processes.Biological research · 2021Article
- 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
- DDIT3 (CHOP) contributes to retinal ganglion cell somal loss but not axonal degeneration in DBA/2J mice.Cell death discovery · 2019Article
- Optic nerve regeneration in the mouse is a complex trait modulated by genetic background.Molecular vision · 2018Article
- BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.Progress in retinal and eye research · 2017Review
- Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The Bcl-2 family is responsible for regulating cell death pathways in neurons during development, after injury and in disease. The activation of the pro-death family member BAX is often the final step before cell death in neurons. Pro-survival family members such as BCL-X (BCL2L1) act to inhibit BAX activation. Overexpression studies have suggested that BCL-X could play an important physiological role in mediating neuronal viability. Loss-of-function studies performed in vivo have implicated BCL-X as a mediator of neuronal survival during the early stages of neurodevelopment. To assess whether BCL-X is needed to promote the survival of neurons in the central nervous system throughout life, Bcl-x was conditionally removed from the optic cup or throughout the adult mouse. During development BCL-X was required for the survival of differentiating retinal ganglion cells (RGCs) leading up to their normal window of developmental death. Despite its expression in adult RGCs, BCL-X was not required for maintaining RGC viability in adult retinas. However, the loss of BCL-X in adult RGCs did significantly increase the rate of death of RGCs after axonal injury. Thus, in developing and injured RGCs there appears to be an active cell survival program preventing neuronal death.
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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.