ArticleCell death and differentiation2007
Regulation of apoptosis by C. elegans CED-9 in the absence of the C-terminal transmembrane domain.
Article in Cell death and differentiation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Endogenous expression and subcellular localization of core apoptosis regulators reveal key differences between embryonic and germline apoptosis in C. elegans.Cell death and differentiation · 2026Article
- Endogenous Expression and Subcellular Localization of Core Apoptosis Regulators Reveal Key Differences Between Embryonic and Germline Apoptosis in C. elegans.Research square · 2026Article
- Fluorescent protein tagging of C. elegans core apoptosis pathway components reveals mitochondrial localization of CED-9 Bcl-2, CED-4 Apaf1 and CED-3 Caspase in non-apoptotic and apoptotic cells.Cell death and differentiation · 2026Article
- Validation of metaxin-2 deficient C. elegans as a model for MandibuloAcral Dysplasia associated to mtx-2 (MADaM) syndrome.Communications biology · 2024Article
- Apoptotic gene loss in Cnidaria is associated with transition to parasitism.Scientific reports · 2023Article
- A Reference Genome ofGenes · 2020Article
- Subcellular Localization and Dynamics of the Bcl-2 Family of Proteins.Frontiers in cell and developmental biology · 2018Review
- Dynamic Control of X Chromosome Conformation and Repression by a Histone H4K20 Demethylase.Cell · 2017Article
- Screening of suppressors of bax-induced cell death identifies glycerophosphate oxidase-1 as a mediator of debcl-induced apoptosis in Drosophila.Genes & cancer · 2015Article
- Cell Death in C. elegans Development.Current topics in developmental biology · 2015Review
- Mitochondrial regulation of cell death.Cold Spring Harbor perspectives in biology · 2013Review
- Hepatitis B virus X protein targets the Bcl-2 protein CED-9 to induce intracellular Ca2+ increase and cell death in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Mitochondria and cell signalling.Journal of cell science · 2012Review
- Article
- The C. elegans B-cell lymphoma 2 (Bcl-2) homolog cell death abnormal 9 (CED-9) associates with and remodels LIPID membranes.Protein science : a publication of the Protein Society · 2011Article
- Caenorhabditis elegans as a model system to study intercompartmental proteostasis: Interrelation of mitochondrial function, longevity, and neurodegenerative diseases.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- The role of mitochondria in apoptosis*.Annual review of genetics · 2009Review
- CED-9 and mitochondrial homeostasis in C. elegans muscle.Journal of cell science · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Bcl-2 proteins regulate apoptosis in organisms as diverse as mammals and nematodes. These proteins are often localized at mitochondria by a C-terminal transmembrane domain. Although the transmembrane domain and mitochondrial localization are centrally involved in specific cases of vertebrate Bcl-2 activity, the significance of this localization is not clear for all species. Studying the Caenorhabditis elegans Bcl-2 homolog CED-9, we found that the transmembrane domain was both necessary and sufficient for localization at mitochondrial outer membranes. Furthermore, we found that in our assays, ced-9 transgenes lacking the transmembrane domain, although somewhat less active than equivalent transgenes derived from wild-type ced-9, rescued embryonic lethality of ced-9(lf) animals and responded properly to upstream signals in controlling the fate of Pn.aap neurons. Both of these apoptotic activities were retained in a construct where CED-9 lacking the transmembrane domain was targeted to the cytosolic surface of the endoplasmic reticulum and derived organelles, suggesting that in wild-type animals, accumulation at mitochondria is not essential for CED-9 to either inhibit or promote apoptosis in C. elegans. Taken together, these data are consistent with a multimodal character of CED-9 action, with an ability to regulate apoptosis through interactions in the cytosol coexisting with additional evolutionarily conserved role(s) at the membrane.
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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.