ArticleProceedings of the National Academy of Sciences of the United States of America2013
Calpain-dependent cytoskeletal rearrangement exploited for anthrax toxin endocytosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- The Multifaceted Role of Calcium Signaling in Regulated Necrosis.Biomolecules · 2025Review
- Advanced glycation end products promote the progression of chronic kidney diseases by targeting calpain 6.Amino acids · 2023Article
- Enterococcus faecalis alters endo-lysosomal trafficking to replicate and persist within mammalian cells.PLoS pathogens · 2022Article
- Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway.Neural plasticity · 2022Article
- The Caenorhabditis elegans CUB-like-domain containing protein RBT-1 functions as a receptor for Bacillus thuringiensis Cry6Aa toxin.PLoS pathogens · 2020Article
- Converging physiological roles of the anthrax toxin receptors.F1000Research · 2019Review
- In vivo induction of membrane damage by β-amyloid peptide oligomers.Acta neuropathologica communications · 2018Article
- A Membrane Potential- and Calpain-Dependent Reversal of Caspase-1 Inhibition Regulates Canonical NLRP3 Inflammasome.Cell reports · 2018Article
- Article
- Endothelial cell calpain as a critical modulator of angiogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Attenuation of Blood-Brain Barrier Breakdown and Hyperpermeability by Calpain Inhibition.The Journal of biological chemistry · 2016Article
- Acquired resistance to innate immune clearance promotesJCI insight · 2016Article
- Cross-inhibition of pathogenic agents and the host proteins they exploit.Scientific reports · 2016Article
- Calpain-6 confers atherogenicity to macrophages by dysregulating pre-mRNA splicing.The Journal of clinical investigation · 2016Article
- The Ins and Outs of Anthrax Toxin.Toxins · 2016Review
- How Shigella Utilizes Ca(2+) Jagged Edge Signals during Invasion of Epithelial Cells.Frontiers in cellular and infection microbiology · 2016Review
- Repurposing FDA approved drugs against the human fungal pathogen, Candida albicans.Annals of clinical microbiology and antimicrobials · 2015Article
- Designing inhibitors of anthrax toxin.Expert opinion on drug discovery · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protective antigen component of Bacillus anthracis toxins can interact with at least three distinct proteins on the host cell surface, capillary morphogenesis gene 2 (CMG2), tumor endothelial marker 8, and β1-integrin, and, with the assistance of other host proteins, enters targeted cells by receptor-mediated endocytosis. Using an antisense-based phenotypic screen, we discovered the role of calpains in this process. We show that functions of a ubiquitous Ca(2+)-dependent cysteine protease, calpain-2, and of the calpain substrate talin-1 are exploited for association of anthrax toxin and its principal receptor, CMG2, with higher-order actin filaments and consequently for toxin entry into host cells. Down-regulated expression of calpain-2 or talin-1, or pharmacological interference with calpain action, did not affect toxin binding but reduced endocytosis and increased the survival of cells exposed to anthrax lethal toxin. Adventitious expression of wild-type talin-1 promoted toxin endocytosis and lethality, whereas expression of a talin-1 mutant (L432G) that is insensitive to calpain cleavage did not. Disruption of talin-1, which links integrin-containing focal adhesion complexes to the actin cytoskeleton, facilitated association of toxin bound to its principal cell-surface receptor, CMG2, with higher-order actin filaments undergoing dynamic disassembly and reassembly during endocytosis. Our results reveal a mechanism by which a bacterial toxin uses constitutively occurring calpain-mediated cytoskeletal rearrangement for internalization.
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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.