ArticleCellular microbiology2007
Alteration of NF-kappaB activity leads to mitochondrial apoptosis after infection with pathological prion protein.
Article in Cellular microbiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Protective role of cytosolic prion protein against virus infection in prion-infected cells.Journal of virology · 2024Article
- Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age.Molecular cancer · 2024Review
- Identification of Novel Circular RNA Targets in Key Penumbra Region of Rats After Cerebral Ischemia-Reperfusion Injury.Journal of molecular neuroscience : MN · 2023Article
- Core transcriptional regulatory circuits in prion diseases.Molecular brain · 2020Article
- Role of Nuclear Factor Kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach.Current neuropharmacology · 2020Review
- Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis.Cell cycle (Georgetown, Tex.) · 2019Article
- Cellular prion protein (PrPOncogene · 2017Article
- Chronic Oxidative Stress, Mitochondrial Dysfunction, Nrf2 Activation and Inflammation in the Hippocampus Accompany Heightened Systemic Inflammation and Oxidative Stress in an Animal Model of Gulf War Illness.Frontiers in molecular neuroscience · 2017Article
- Identifying Novel Candidate Genes Related to Apoptosis from a Protein-Protein Interaction Network.Computational and mathematical methods in medicine · 2015Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Bcl-3 regulates UVB-induced apoptosis.Human cell · 2013Article
- Lentiviral delivery of RNAi for in vivo lineage-specific modulation of gene expression in mouse lung macrophages.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.Infection and immunity · 2011Article
- Article
- Expression profile of human gingival fibroblasts induced by interleukin-1beta reveals central role of nuclear factor-kappa B in stabilizing human gingival fibroblasts during inflammation.Journal of periodontology · 2009Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor kappa B (NF-kappaB) is a key regulator of the immune response, but in almost the same manner it is involved in induction of inflammation, proliferation and regulation of apoptosis. In the central nervous system activated NF-kappaB plays a neuroprotective role. While in some neurodegenerative disorders the role of NF-kappaB is well characterized, there is poor knowledge on the role of NF-kappaB in prion disease. We found binding but no transcriptional activity of the transcription factor in vitro. Characterizing the mechanism of cell death after infection with pathological prion protein increased caspase-9 and caspase-3 activity was detected and the lack of NF-kappaB activity resulted in the inability to activate target genes that usually play an important role in neuroprotection. Additionally, we investigated the role of NF-kappaB after prion infection of Nfkb1(-/-), Nfkb2(-/-) and Bcl3(-/-) mice and central nervous system-specific p65-deleted mice revealing an accelerated prion disease in NF-kappaB2- and Bcl-3-deficient mice, which is in line with a reduced neuroprotective activity in prion infection. Based on our findings, we propose a model whereby the alteration of NF-kappaB activity at the early stages of infection with pathological prion protein leads to neuronal cell death mediated by mitochondrial apoptosis.
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