ArticleProceedings of the National Academy of Sciences of the United States of America2002
DT40 cells lacking the Ca2+-binding protein annexin 5 are resistant to Ca2+-dependent apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 57 citations in OpenAlex.
- Annexin A5 Maintains Mitochondrial Integrity by Inhibiting mPTP Opening to Protect Against Acetaminophen-Induced Acute Liver Injury.International journal of molecular sciences · 2026Article
- The Relevance, Predictability, and Utility of Annexin A5 for Human Physiopathology.International journal of molecular sciences · 2024Review
- A Temporal Comparative RNA Transcriptome Profile of the Annexin Gene Family in the Salivary versus Lacrimal Glands of the Sjögren's Syndrome-Susceptible C57BL/6.NOD-International journal of molecular sciences · 2022Article
- Annexins and cardiovascular diseases: Beyond membrane trafficking and repair.Frontiers in cell and developmental biology · 2022Review
- Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021Review
- AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer CellsFrontiers in oncology · 2021Article
- Prognostic Significance of Increased Expression of Annexin A10 (ANXA10) in Serous Epithelial Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- 3,5-Diiodo-L-Thyronine Exerts Metabolically Favorable Effects on Visceral Adipose Tissue of Rats Receiving a High-Fat Diet.Nutrients · 2019Article
- Annexin A5 overexpression might suppress proliferation and metastasis of human uterine cervical carcinoma cells.Cancer biomarkers : section A of Disease markers · 2018Article
- Article
- Differential in gel electrophoresis (DIGE) comparative proteomic analysis of macrophages cell cultures in response to perthamide C treatment.Marine drugs · 2013Article
- Regulation of mitochondrial morphogenesis by annexin A6.PloS one · 2013Article
- Enhanced charge-independent mitochondrial free Ca(2+) and attenuated ADP-induced NADH oxidation by isoflurane: Implications for cardioprotection.Biochimica et biophysica acta · 2012Article
- Article
- Proteome alteration induced by hTERT transfection of human fibroblast cells.Proteome science · 2008Article
- Biological modulation by lectins and their ligands in tumor progression and metastasis.Anti-cancer agents in medicinal chemistry · 2008Review
- The use of genetic programming in the analysis of quantitative gene expression profiles for identification of nodal status in bladder cancer.BMC cancer · 2006Article
- Antagonist of growth hormone-releasing hormone induces apoptosis in LNCaP human prostate cancer cells through a Ca2+-dependent pathway.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Annexin A5 is not essential for skeletal development.Molecular and cellular biology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Annexins are widely expressed Ca(2+)-dependent phospholipid-binding proteins with poorly understood physiological roles. Proposed functions include Ca(2+) channel activity and vesicle trafficking, but neither have been proven in vivo. Here we used targeted gene disruption to generate B-lymphocytes lacking annexin 5 (Anx5) expression and show that this results in reduced susceptibility to a range of apoptotic stimuli. By comparison B-lymphocytes lacking annexin 2 (Anx2) showed no such resistance, providing evidence that this effect is specific to loss of Anx5. The defect in the ANX5(-/-) cells occurs early in the apoptotic program before nuclear condensation, caspase 3 activation, and cell shrinkage, but downstream of an initial Ca(2+) influx. Only UVA/B irradiation induced similar levels of apoptosis in wild-type and ANX5(-/-) cells. Unexpectedly, ANX5(-/-) cells permeabilized in vitro also failed to release mitochondrial cytochrome C, suggesting a possible mechanism for their resistance to apoptosis. These findings demonstrate a role for Anx5 in determining the susceptibility of B-lymphocytes to apoptosis.
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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.