Evidence map›Paper›PMID 41476654›Full record

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.

Fangfang Liu, Zhong-Da Li, Yanqiao Zeng, Xiaofeng Wang, Yingnan Liu, Qi Li, Wenhe Luo, Xiaoman Suo, Yaqing Xu, Feng Yuan and 6 more

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Fangfang LiuLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Zhong-Da LiLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Yanqiao ZengLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Xiaofeng WangLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Yingnan LiuLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Qi LiLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Wenhe LuoLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Xiaoman SuoLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Yaqing XuLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Feng YuanLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Dan ZhangLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Wuqiong ZhangLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Shengyong GengMaterials and Interfaces Center Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.ORCID https://orcid.org/0000-0003-4386-2092
Xue-Feng YuMaterials and Interfaces Center Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Guofang ZhangLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.
Yang LiLaboratory of Inflammation and Vaccines Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen China.ORCID https://orcid.org/0000-0001-7242-4687

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

black phosphorus nanomaterialsPLK1 inhibitorPLK familyprotein structuretargeted interaction of nanomaterial with protein

Identifiers

PMID41476654
PMCPMC12752640

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.