ArticlePloS one2012
BAT3 regulates Mycobacterium tuberculosis protein ESAT-6-mediated apoptosis of macrophages.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer.Journal of the National Cancer Institute · 2015Pooled it
- Trial
- Immunoregulation by ESAT-6: From Pathogenesis of Tuberculosis to Potential Anti-Inflammatory and Anti-Rejection Application.Pharmaceuticals (Basel, Switzerland) · 2025Review
- ESAT-6 Modulates Macrophage Apoptosis in Mycobacterium Tuberculosis via lncNEAT1/miR-125b-5p/TNF-α Pathway.Infection and drug resistance · 2025Article
- Dissecting the pathogenic effects of smoking in blood DNA methylation on allergic diseases.The World Allergy Organization journal · 2024Article
- Mycobacterium tuberculosis virulence protein ESAT-6 influences M1/M2 polarization and macrophage apoptosis to regulate tuberculosis progression.Genes & genomics · 2024Article
- ESAT-6 a Major Virulence Factor ofBiomolecules · 2023Review
- An N-acetyltransferase required for EsxA N-terminal protein acetylation and virulence in Mycobacterium marinum.bioRxiv : the preprint server for biology · 2023Article
- A Small Protein but with Diverse Roles: A Review of EsxA in Mycobacterium-Host Interaction.Cells · 2021Review
- Article
- Early secreted antigenic target of 6-kDa of Mycobacterium tuberculosis promotes caspase-9/caspase-3-mediated apoptosis in macrophages.Molecular and cellular biochemistry · 2019Article
- A Decade of GWAS Results in Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Review
- Article
- Constitutive expression of SMAR1 confers susceptibility to Mycobacterium tuberculosis infection in a transgenic mouse model.The Indian journal of medical research · 2015Article
- Overexpression of BAT3 alleviates prion protein fragment PrP106-126-induced neuronal apoptosis.CNS neuroscience & therapeutics · 2014Article
- Bim is a crucial regulator of apoptosis induced by Mycobacterium tuberculosis.Cell death & disease · 2014Article
- BAG-6, a jack of all trades in health and disease.Cellular and molecular life sciences : CMLS · 2014Review
- Cell death paradigms in the pathogenesis of Mycobacterium tuberculosis infection.Frontiers in cellular and infection microbiology · 2014Review
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HLA-B-associated transcript 3 (BAT3), also known as Scythe or BAG6, is a nuclear protein implicated in the control of apoptosis and natural killer (NK) cell-dendritic cell (DC) interaction. We demonstrate that BAT3 modulates the immune response by regulating the function of macrophages. BAT3 is released by macrophages in vitro and it down-regulates nitric oxide and proinflammatory cytokines release in IFN-γ and LPS stimulated macrophages. Furthermore, Mycobacterium tuberculosis-derived protein ESAT-6 (Rv3875) induced transient increase in the expression and release of BAT3 in macrophages. We show that induction of apoptosis by ESAT-6 is dependent on the cleavage of BAT3 by caspase-3 and proteasomal degradation. Our results also indicate that BAT3 regulates ESAT-6-induced apoptosis by interacting with anti-apoptotic protein BCL-2. Taken together, the data suggest that BAT3 plays a role in the early immune response to M. tuberculosis infection and may be a key protein associated with the fate of antigen presenting cells during infection.
Indexed as
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What OpenQuestion holds
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.