ArticleScientific reports2016
Cellular uptake of exogenous calcineurin B is dependent on TLR4/MD2/CD14 complexes, and CnB is an endogenous ligand of TLR4.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- β-chitosan attenuates hepatic macrophage-driven inflammation and reverses aging-related cognitive impairment.iScience · 2024Article
- Cytotoxic Effect ofAdvances in pharmacological and pharmaceutical sciences · 2024Article
- Pyroptosis in renal inflammation and fibrosis: current knowledge and clinical significance.Cell death & disease · 2023Review
- rhCNB Improves Cyclophosphamide-Induced Immunodeficiency in BALB/c Mice.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- In Silico Characterization of Calcineurin from Pathogenic Obligate Intracellular Trypanosomatids: Potential New Biological Roles.Biomolecules · 2021Article
- Article
- The immunostimulatory effects and pro-apoptotic activity of rhCNB against Lewis lung cancer is mediated by Toll-like receptor 4.Cancer medicine · 2019Article
- Prognostic predictive value of TLR4 polymorphisms in Han Chinese population with hypertrophic cardiomyopathy.The Kaohsiung journal of medical sciences · 2018Article
- The genetically engineered drug rhCNB induces apoptosis via a mitochondrial route in tumor cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous research showed that recombinant calcineurin B (rhCnB) stimulates cytokine secretion by immune cells, probably through TLR4. Exogenous CnB can be incorporated into many different tumour cells in vitro, but the mode of uptake and receptors required remain unknown. Here, we report that exogenous CnB is taken up by cells in a time- and concentration-dependent manner via clathrin-dependent receptor-mediated internalization. Our findings further confirm that uptake is mediated by the TLR4/MD2 complex together with the co-receptor CD14. The MST results revealed a high affinity between CnB and the TLR4 receptor complex. No binding was detected between CnB and LPS. CnB inhibited the uptake of LPS, and LPS also inhibited the uptake of CnB. These results indicate that the uptake of exogenous CnB did not occur through LPS and that CnB was not a chaperone of LPS. Thus, we conclude that TLR4 receptor complexes were required for the recognition and internalization of exogenous CnB. CnB could be a potential endogenous ligand of TLR4 and function as an agonist of TLR4. These properties of CnB support its potential for development as an anti-cancer drug.
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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.