STK39-mediated amplification of γ-H2A.X promotes homologous recombination and contributes to PARP inhibitor resistance
Yi Xu, Changying Li, Huan Yin, Somaira Nowsheen, Xin Xu, Wenjuan Kang, Xin Liu, Lifeng Chen, Zhenkun Lou, Junlin Yi, Min Deng · 2024
Read STK39-mediated amplification of γ-H2A.X promotes homologous recombination and contributes to PARP inhibitor resistance by Yi Xu, Changying Li, Huan Yin, Somaira Nowsheen, Xin Xu, Wenjuan Kang, Xin Liu, Lifeng Chen, Zhenkun Lou, Junlin Yi, Min Deng (2024) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-11662673.txt.
Description
Yi Xu and co-authors report a 2024 study on how cells fix broken DNA and why some tumors resist a class of drugs. When DNA breaks, a protein mark called gamma-H2A.X flags the damage and calls in repair crews. A kinase named ATM was long seen as the main source of that mark.
The team found a second kinase, STK39, that boosts the mark after damage. STK39 joins the repair complex at the break site and adds more marks, which speeds repair by gene copying. Pancreatic tumors with high STK39 resisted PARP inhibitor drugs. Blocking STK39 while giving those drugs shrank tumors and undid resistance in tests. The pair of drugs may help patients whose tumors no longer respond.
Catalog record
| CREATOR | Yi Xu, Changying Li, Huan Yin, Somaira Nowsheen, Xin Xu, Wenjuan Kang, Xin Liu, Lifeng Chen, Zhenkun Lou, Junlin Yi, Min Deng |
|---|---|
| YEAR | 2024 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 51 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |