ArticleBlood2009
Selective roles for antiapoptotic MCL-1 during granulocyte development and macrophage effector function.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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.
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
74 citing papers in PubMed, 119 citations in OpenAlex.
- Effects of the pan-caspase inhibitor Q-VD-OPh on human neutrophil lifespan and function.PloS one · 2025Article
- Neutrophils negatively control IL-17A-producing γδ T cell frequencies in a contact-dependent manner under physiological conditions.Frontiers in immunology · 2025Article
- Review
- Anti-apoptotic MCL-1 promotes long-chain fatty acid oxidation through interaction with ACSL1.Molecular cell · 2024Article
- NET formation is a default epigenetic program controlled by PAD4 in apoptotic neutrophils.Science advances · 2023Article
- A1 is induced by pathogen ligands to limit myeloid cell death and NLRP3 inflammasome activation.EMBO reports · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- What can we learn from mice lacking pro-survival BCL-2 proteins to advance BH3 mimetic drugs for cancer therapy?Cell death and differentiation · 2022Review
- Filanesib plus bortezomib and dexamethasone in relapsed/refractory t(11;14) and 1q21 gain multiple myeloma.Cancer medicine · 2022Article
- Monocytes Elicit a Neutrophil-Independent Th1/Th17 Response Upon Immunization With a Mincle-Dependent Glycolipid Adjuvant.Frontiers in immunology · 2022Article
- The multiple mechanisms of MCL1 in the regulation of cell fate.Communications biology · 2021Review
- Therapeutics Targeting the Core Apoptotic Machinery.Cancers · 2021Review
- Article
- Targeting the CCL2/CCR2 Axis in Cancer Immunotherapy: One Stone, Three Birds?Frontiers in immunology · 2021Review
- Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021Review
- Neutrophil infiltration regulates clock-gene expression to organize daily hepatic metabolism.eLife · 2020Article
- Mast Cells in Liver Fibrogenesis.Cells · 2019Review
- Low human and murine Mcl-1 expression leads to a pro-apoptotic plaque phenotype enriched in giant-cells.Scientific reports · 2019Article
- Mcl-1 and Bcl-xL are essential for survival of the developing nervous system.Cell death and differentiation · 2019Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During hematopoiesis, myeloid cell leukemia-1 (MCL-1) mediates the survival of bone marrow progenitors and lymphocytes. However, its requirement during myeloid cell differentiation, development, and effector function is less clear. Lineage-specific deletion of MCL-1 in myeloid precursors results in neutropenia due to death during differentiation. The loss of mature neutrophils induced by Mcl-1 deletion was not rescued by genetic deletion of proapoptotic Bim and Puma or by exogenous cytokine treatment. However, blockade of intrinsic apoptosis by lineage-specific deletion of both multidomain proapoptotics Bax and Bak was capable of rescuing the neutropenia associated with Mcl-1 deletion. In the monocytic lineage, despite efficient Mcl-1 deletion, monocytes and macrophages undergo normal development. During the phagocytosis of extracellular bacteria, macrophages concomitantly increase the expression of both MCL-1 and BIM. However, Mcl-1-deficient macrophages exhibit increased sensitivity to death during bacterial phagocytosis that can be abolished by codeletion of Bim. These data suggest that MCL-1 may be necessary to antagonize BIM during macrophage effector responses. Thus, MCL-1 plays selective roles in myeloid development, being required for neutrophil development and setting the threshold for apoptosis during a macrophage effector response.
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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.