ArticleCell death & disease2024
Contribution of A1 to macrophage survival in cooperation with MCL-1 and BCL-X
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Multiorgan Molecular Landscape of Severe COVID-19 Revealed by Consensus Gene Signatures and RAB8B Targeting.Journal of medical virology · 2026Article
- Identification and validation of candidate biomarkers associated with mitochondria and 18 types of programmed cell death in trigeminal neuralgia: insights from transcriptome sequencing.Frontiers in molecular neuroscience · 2026Article
- Oxidative stress-related biomarkers in thyroid eye disease: evidence from bioinformatics analysis and experimental validation.Frontiers in immunology · 2025Article
- Loss of OScientific reports · 2024Article
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Authors and funding
3 authors.
Funding
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Abstract
Myeloid cells are the first line of defence against pathogens. Mitochondrial apoptosis signalling is a crucial regulator of myeloid cell lifespan and modulates the function of myeloid cells. The anti-apoptotic protein BCL-2-family protein BCL2A1/A1/BFL-1 is strongly upregulated in inflammation in macrophages. We analysed the contribution of A1 to apoptosis regulation in a conditional system of in vitro differentiation of murine macrophages from immortalised progenitors. We disabled the expression of A1 by targeting all murine A1 isoforms in the genome. Specific inhibitors were used to inactivate other anti-apoptotic proteins. Macrophage progenitor survival mainly depended on the anti-apoptotic proteins MCL-1, BCL-X
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