ArticleCell death & disease2015
Impact of the combined loss of BOK, BAX and BAK on the hematopoietic system is slightly more severe than compound loss of BAX and BAK.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 34 citations in OpenAlex.
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Integrating QSP and ML to Facilitate Drug Development and Personalized Medicine.Handbook of experimental pharmacology · 2025Review
- Article
- Apoptotic dysregulation mediates stem cell competition and tissue regeneration.Nature communications · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Exploring the Therapeutic Potentials of Exopolysaccharides Derived From Lactic Acid Bacteria and Bifidobacteria: Antioxidant, Antitumor, and Periodontal Regeneration.Frontiers in microbiology · 2022Article
- Endogenous Bok is stable at the endoplasmic reticulum membrane and does not mediate proteasome inhibitor-induced apoptosis.Frontiers in cell and developmental biology · 2022Article
- Luteolin Alleviates Methamphetamine-Induced Hepatotoxicity by Suppressing the p53 Pathway-Mediated Apoptosis, Autophagy, and Inflammation in Rats.Frontiers in pharmacology · 2021Article
- BAX, BAK, and BOK: A Coming of Age for the BCL-2 Family Effector Proteins.Cold Spring Harbor perspectives in biology · 2020Review
- The Multifaceted Roles of the BCL-2 Family Member BOK.Frontiers in cell and developmental biology · 2020Review
- Designing combination therapies with modeling chaperoned machine learning.PLoS computational biology · 2019Article
- Intrinsic Instability of BOK Enables Membrane Permeabilization in Apoptosis.Cell reports · 2018Article
- Targeting BCL-2 regulated apoptosis in cancer.Open biology · 2018Review
- BOK promotes chemical-induced hepatocarcinogenesis in mice.Cell death and differentiation · 2018Article
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.Cell death and differentiation · 2018Review
- The BAX/BAK-like protein BOK is a prognostic marker in colorectal cancer.Cell death & disease · 2018Article
- How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?Cell death and differentiation · 2018Review
- Viewing BCL2 and cell death control from an evolutionary perspective.Cell death and differentiation · 2018Review
- BOK displays cell death-independent tumor suppressor activity in non-small-cell lung carcinoma.International journal of cancer · 2017Article
- BCL-2 family: integrating stress responses at the ER to control cell demise.Cell death and differentiation · 2017Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that BAX and BAK play crucial, overlapping roles in the intrinsic pathway of apoptosis. Gene targeted mice lacking both BAX and BAK have previously been generated, but the majority of these animals died perinatally. BOK is a poorly studied relative of BAX and BAK that shares extensive amino acid sequence homology to both proteins, but its function remains largely unclear to date. To determine whether BOK plays an overlapping role with BAX and BAK, we utilized a hematopoietic reconstitution model where lethally irradiated wild type mice were transplanted with Bok(-/-)Bax(-/-)Bak(-/-) triple knockout (TKO) fetal liver cells, and compared alongside mice reconstituted with a Bax(-/-)Bak(-/-) double knockout (DKO) hematopoietic compartment. We report here that mice with a TKO and DKO hematopoietic system died at a similar rate and much earlier than control animals, mostly due to severe autoimmune pathology. Both TKO and DKO reconstituted mice also had altered frequencies of various leukocyte subsets in the thymus, bone marrow and spleen, displayed leukocyte infiltrates and autoimmune pathology in multiple tissues, as well as elevated levels of anti-nuclear autoantibodies. Interestingly, the additional deletion of BOK (on top of BAX and BAK loss) led to a further increase in peripheral blood lymphocytes, as well as enhanced lymphoid infiltration in some organs. These findings suggest that BOK may have some functions that are redundant with BAX and BAK in the hematopoietic system.
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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.