IGF1R promotes radiation-induced HSCs activation by regulating DNA-PKcs-mediated DNA damage repair
Our findings suggest that the inhibition of the IGF1R-promoted, DNA-PKcs-dependent non-homologous end joining (NHEJ) repair mode is a promising strategy to prevent the activation of HSCs. To the best of our knowledge, the present study is pioneering in its exploration of the mechanism by which IGF1R mediates radiation-induced activation of HSCs by regulating DNA-PKcs.
Authors
- Gang Zhao (ORCID: https://orcid.org/0000-0001-8142-3037)
- Yan Shen (ORCID: https://orcid.org/0000-0002-7883-5169)
- Chang Liu (ORCID: https://orcid.org/0000-0002-9441-193X)
- Jiajing Li (ORCID: https://orcid.org/0000-0001-7642-5169)
- Yunyun Cheng
- Jie Feng
- Chaonan Sun (ORCID: https://orcid.org/0009-0000-8319-7256)
- Jiguo Lin
Institutions
- Jilin University (CN)
Publication Details
- Journal
- Frontiers in Cell and Developmental Biology
- Published
- 2025-11-14
- DOI
- https://doi.org/10.3389/fcell.2025.1678654
- Primary Topic
- DNA Repair Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- People's Government of Jilin Province
- Jilin University