ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Diminishing apoptosis by deletion of Bax or overexpression of Bcl-2 does not protect against infectious prion toxicity in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Kola nut from Cola nitida vent. Schott administered to pregnant rats induces histological alterations in pups' cerebellum.PloS one · 2021Article
- What Is Our Current Understanding of PrPPathogens (Basel, Switzerland) · 2017Review
- Prion infections and anti-PrP antibodies trigger converging neurotoxic pathways.PLoS pathogens · 2015Article
- Activation of pro-survival CaMK4β/CREB and pro-death MST1 signaling at early and late times during a mouse model of prion disease.Virology journal · 2014Article
- Cytosolic caspases mediate mislocalised SOD2 depletion in an in vitro model of chronic prion infection.Disease models & mechanisms · 2013Article
- Synaptic dysfunction in prion diseases: a trafficking problem?International journal of cell biology · 2013Review
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- The intricate mechanisms of neurodegeneration in prion diseases.Trends in molecular medicine · 2011Review
- Engulfment of cerebral apoptotic bodies controls the course of prion disease in a mouse strain-dependent manner.The Journal of experimental medicine · 2010Article
- A highly toxic cellular prion protein induces a novel, nonapoptotic form of neuronal death.The American journal of pathology · 2010Article
- Degenerating synaptic boutons in prion disease: microglia activation without synaptic stripping.The American journal of pathology · 2009Article
- Cytoplasmic prion protein induces forebrain neurotoxicity.Biochimica et biophysica acta · 2009Article
- The role of calorie restriction and SIRT1 in prion-mediated neurodegeneration.Experimental gerontology · 2008Article
- Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Prion protein lacks robust cytoprotective activity in cultured cells.Molecular neurodegeneration · 2008Article
- All quiet on the neuronal front: NMDA receptor inhibition by prion protein.The Journal of cell biology · 2008Article
- Unfolded protein response transcription factor XBP-1 does not influence prion replication or pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
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Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
B-cell lymphoma protein 2 (Bcl-2) and Bcl-2-associated X protein (Bax), key antiapoptotic and proapoptotic proteins, respectively, have important roles in acute and chronic models of neurologic disease. Several studies have implicated Bax and Bcl-2 in mediating neurotoxicity in prion diseases. To determine whether diminishing apoptotic cell death is protective in an infectious prion disease model we inoculated mice that either were null for proapoptotic Bax or overexpressed antiapoptotic Bcl-2. Interestingly, genetic manipulation of apoptosis did not lessen the clinical severity of disease. Moreover, some disease parameters, such as behavioral alterations and death, occurred slightly earlier in mice that are null for Bax or overexpress Bcl-2. These results suggest that Bax and Bcl-2 mediated apoptotic pathways are not the major contributing factor to the clinical or pathological features of infectious prion disease.
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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.