ArticleBlood2014
Deregulated cell death and lymphocyte homeostasis cause premature lethality in mice lacking the BH3-only proteins Bim and Bmf.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 47 citations in OpenAlex.
- Limited roles of the miR-17-92 cluster in the regulation of T-cell apoptosis.The FEBS journal · 2026Article
- Bcl-2 modifying factor (Bmf): "a mysterious stranger" in the Bcl-2 family proteins.Cell death and differentiation · 2026Review
- PUMA-induced apoptosis drives bone marrow failure and genomic instability in telomerase-deficient mice.Cell death and differentiation · 2026Article
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Survival and Developmental Progression of Unselected Thymocytes in the Absence of the T-Cell Adaptor Gads.European journal of immunology · 2025Article
- Chronic spindle assembly checkpoint activation causes myelosuppression and gastrointestinal atrophy.EMBO reports · 2024Article
- The thymus road to a T cell: migration, selection, and atrophy.Frontiers in immunology · 2024Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Structural basis of the specificity and interaction mechanism of Bmf binding to pro-survival Bcl-2 family proteins.Computational and structural biotechnology journal · 2023Article
- The transcription factor IRF4 represses proapoptotic BMF and BIM to licence multiple myeloma survival.Leukemia · 2021Article
- Loss of BIM in T cells results in BCL-2 family BH3-member compensation but incomplete cell death sensitivity normalization.Apoptosis : an international journal on programmed cell death · 2020Article
- Dynein light chain binding determines complex formation and posttranslational stability of the Bcl-2 family members Bmf and Bim.Cell death and differentiation · 2020Article
- The essentials of developmental apoptosis.F1000Research · 2020Review
- CHK1 dosage in germinal center B cells controls humoral immunity.Cell death and differentiation · 2019Article
- Identification of a genomic enhancer that enforces proper apoptosis induction in thymic negative selection.Nature communications · 2019Article
- c-Myb Coordinates Survival and the Expression of Genes That Are Critical for the Pre-BCR Checkpoint.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Targeting BCL-2 regulated apoptosis in cancer.Open biology · 2018Review
- Perturbing mitosis for anti-cancer therapy: is cell death the only answer?EMBO reports · 2018Review
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.Cell death and differentiation · 2018Review
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
BH3 domain-only proteins (BH3-only) proteins are members of the Bcl-2 family that play crucial roles in embryogenesis and the maintenance of tissue homeostasis by triggering apoptotic cell death. The BH3-only protein Bim is critical for developmental apoptosis of lymphocytes, securing establishment of tolerance and for the termination of immune responses. Bim is believed to act in concert with other BH3-only proteins or members of the tumor necrosis factor receptor family in getting rid of unwanted cells. Bmf, a related BH3-only protein, was shown to play a role in B-cell homeostasis and to mediate cell death in response to certain apoptotic triggers, including glucocorticoid, histone deacetylase inhibitors, and overexpression of the c-Myc proto-oncogene. Here we show that Bim and Bmf have overlapping functions during mouse development and coregulate lymphocyte homeostasis and apoptosis in a nonredundant manner. Double deficiency of Bim and Bmf caused more B lymphadenopathy than loss of either BH3-only protein alone, and this was associated with autoimmune glomerulonephritis and a range of malignancies in aged mice. Thus, our results demonstrate that Bim and Bmf act in concert to prevent autoimmunity and malignant disease, strengthening the rational for the development of BH3-only protein mimicking therapeutics for the treatment of such disorders.
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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.