AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
Powered by AMiner. Clicking this button will take you away from SciOpen.
Home Genes & Diseases Article
PDF (4.1 MB)
Cite
EndNote(RIS) BibTeX
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Rapid Communication | Open Access

Ribonucleotide reductase M1 regulates the cell cycle via minichromosome maintenance proteins

Agnes Malysaa,c, Jenny M. Kreahlingb,c, Scott N. Freemanb,c, Bin Baoa, Jiawei Zhaoa, Xiaohong Zhanga, Manohar Ratnama, Gerold Beplera,b( )
Karmanos Cancer Institute and Department of Oncology, Wayne State University, Detroit, MI 48201, USA
Department of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA

c These authors contributed equally to this work.

Peer review under the responsibility of Chongqing Medical University.

Show Author Information

References

【1】
【1】
 
 
Crossref Google Scholar
Genes & Diseases
Volume 13 Issue 4,
July 2026
DOI: 10.1016/j.gendis.2025.101927

{{item.num}}

Comments on this article

Go to comment

< Back to all reports

Review Status: {{reviewData.commendedNum}} Commended , {{reviewData.revisionRequiredNum}} Revision Required , {{reviewData.notCommendedNum}} Not Commended Under Peer Review

Review Comment

Cite this Report
Close
Close
Cite this article:
Malysa A, Kreahling JM, Freeman SN, et al. Ribonucleotide reductase M1 regulates the cell cycle via minichromosome maintenance proteins. Genes & Diseases, 2026, 13(4). https://doi.org/10.1016/j.gendis.2025.101927

5

Views

0

Downloads

0

Crossref

0

Web of Science

0

Scopus

0

CSCD
Received: 22 January 2025
Published: 08 November 2025
© 2025 The Authors.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).