ArticleExploration (Beijing, China)2025
Target Binding of Black Phosphorus Nanomaterial to Polo-Like Kinase 1 for Cancer Chemotherapy: A Mutual Selection of Nanomaterial and Protein.
Article in Exploration (Beijing, China), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Nanomedicine-based cancer immunotherapy: translational barriers, mechanistic strategies, and future perspectives.Drug delivery · 2026Review
- Target Binding of Black Phosphorus Nanomaterial to Polo-Like Kinase 1 for Cancer Chemotherapy: A Mutual Selection of Nanomaterial and Protein.Exploration (Beijing, China) · 2025Article
- Designing nanoparticles to minimize unintended inflammatory responses: a step toward safer and more effective precision nanomedicine.Nanomedicine (London, England) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intrinsic properties of black phosphorus (BP) nanomaterials (NMs) enable them for targeted binding to polo-like kinase 1 (PLK1), thus inhibiting its kinase activity. However, the mechanism and targeted binding sites underlying this interaction remain unclear. To elucidate the critical properties of PLK1 that facilitate its interaction with BPNMs, the binding ability of BPNMs was compared across PLK family proteins. Although BPNMs exhibited a weak binding affinity for PLK3, PLK1 demonstrated the most favorable physicochemical properties for its binding. Factors as surface charge, hydrophobicity, secondary and three-dimensional structures significantly affected the interaction of PLK family proteins to BPNMs. The binding affinity was primarily determined by amino acid residues at the binding interface, where arginine and proline played critical roles in mediating the interaction of BPNMs-PLK1. BPNMs inhibited PLK1 activation by binding to key residues of the kinase domain, including S49, Y203, D204, E206, and R207. In conclusion, this study elucidates the molecular basis of the specific interaction between BPNMs and PLK1, highlighting the pivotal role of the amino acid residues in NM-protein binding. This work demonstrates that NM-protein interactions are a mutual selection and driven by the physicochemical properties of both proteins and NMs.
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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.