ArticleMolecular and cellular biology2004
Proapoptotic BH3-only Bcl-2 family member Bik/Blk/Nbk is expressed in hemopoietic and endothelial cells but is redundant for their programmed death.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
64 citing papers in PubMed, 114 citations in OpenAlex.
- Persistence of emphysema following cessation of cigarette smoke exposure requires a susceptibility factor.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Bik promotes proteasomal degradation to control low-grade inflammation.The Journal of clinical investigation · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Independent role of caspases and Bik in augmenting influenza A virus replication in airway epithelial cells and mice.Virology journal · 2023Article
- Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023Review
- Casein kinase II activates Bik to induce death of hyperplastic mucous cells in a cell cycle-dependent manner.Journal of cellular physiology · 2022Article
- Contribution of cell death signaling to blood vessel formation.Cellular and molecular life sciences : CMLS · 2021Review
- The third model of Bax/Bak activation: a Bcl-2 family feud finally resolved?F1000Research · 2020Review
- The essentials of developmental apoptosis.F1000Research · 2020Review
- Activity-Dependent Regulation of the Proapoptotic BH3-Only GeneG3 (Bethesda, Md.) · 2019Article
- IL-13 in LPS-Induced Inflammation Causes Bcl-2 Expression to Sustain Hyperplastic Mucous cells.Scientific reports · 2018Article
- Targeting the Bcl-2 Family in B Cell Lymphoma.Frontiers in oncology · 2018Review
- Does the BCL-2 family member BIK control lung carcinogenesis?Molecular & cellular oncology · 2018Article
- Endothelial cell apoptosis in angiogenesis and vessel regression.Cellular and molecular life sciences : CMLS · 2017Review
- Bik reduces hyperplastic cells by increasing Bak and activating DAPk1 to juxtapose ER and mitochondria.Nature communications · 2017Article
- Engineered myocardium model to study the roles of HIF-1α and HIF1A-AS1 in paracrine-only signaling under pathological level oxidative stress.Acta biomaterialia · 2017Article
- Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice.Clinical and experimental immunology · 2017Article
- BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.Progress in retinal and eye research · 2017Review
- Interrogating the relevance of mitochondrial apoptosis for vertebrate development and postnatal tissue homeostasis.Genes & development · 2016Review
- Osteopontin-stimulated apoptosis in cardiac myocytes involves oxidative stress and mitochondrial death pathway: role of a pro-apoptotic protein BIK.Molecular and cellular biochemistry · 2016Article
4 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 1 institution in 1 country.
Funding
Abstract
The BH3-only members of the Bcl-2 protein family are essential for initiation of programmed cell death and stress-induced apoptosis. We have determined the expression pattern in mice of the BH3-only protein Bik, also called Blk or Nbk, and examined its physiological function by gene targeting. We found that Bik is expressed widely in the hematopoietic compartment and in endothelial cells of the venous but not arterial lineages. Nevertheless, its loss did not increase the numbers of such cells in mice or protect hematopoietic cells in vitro from apoptosis induced by cytokine withdrawal or diverse other cytotoxic stimuli. Moreover, whereas loss of the BH3-only protein Bim rescued mice lacking the prosurvival protein Bcl-2 from fatal polycystic kidney disease and lymphopenia, loss of Bik did not. These results indicate that any function of Bik in programmed cell death and stress-induced apoptosis must overlap that of other BH3-only proteins.
Indexed as
Identifiers
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.