ArticleCommunications biology2022
LDLR, LRP1, and Megalin redundantly participate in the uptake of Clostridium novyi alpha-toxin.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- LDL receptor-mediated endocytosis ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Clostridial Myonecrosis: A Comprehensive Review of Toxin Pathophysiology and Management Strategies.Microorganisms · 2024Review
- Identification of a hemorrhagic determinant inMicrobiology spectrum · 2024Article
- Molecular basis of TMPRSS2 recognition by Paeniclostridium sordellii hemorrhagic toxin.Nature communications · 2024Article
- Structural dynamics of the CROPs domain control stability and toxicity of Paeniclostridium sordellii lethal toxin.Nature communications · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium novyi alpha-toxin (Tcnα) is a potent exotoxin that induces severe symptoms including gas gangrene, myositis, necrotic hepatitis, and sepsis. Tcnα binds to sulfated glycosaminoglycans (sGAG) for cell-surface attachment and utilizes low-density lipoprotein receptor (LDLR) for rapid entry. However, it was also shown that Tcnα may use alternative entry receptors other than LDLR. Here, we define that LRP1 and Megalin can also facilitate the cellular entry of Tcnα by employing reconstitutive LDLR family proteins. LDLR, LRP1, and Megalin recognize Tcnα via their ligand-binding domains (also known as LDL receptor type A repeats). Notably, LDLR and LRP1 have contrasting expression levels in many different cells, thus the dominant entry receptor for Tcnα could be cell-type dependent. These findings together increase our knowledge of the Tcnα actions and further help to understand the pathogenesis of C. novyi infection-associated diseases.
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Registered trials
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