Fork restart: unloading FANCD2 to travel ahead.

Autor:	Iyer DR; Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA., D'Andrea AD; Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: alan_dandrea@dfci.harvard.edu.
Jazyk:	angličtina
Zdroj:	Molecular cell [Mol Cell] 2023 Oct 19; Vol. 83 (20), pp. 3590-3592.
DOI:	10.1016/j.molcel.2023.09.027
Abstrakt:	In this issue of Molecular Cell, Brunner et al. 1 reveal that eliminating FANCD2 from stalled forks via FBXL12-mediated degradation enables cells to tolerate oncogene-induced replication stress, making FBXL12 a promising target for cancer treatment. Competing Interests: Declaration of interests A.D.D. reports consulting for AstraZeneca, Bayer AG, Bristol Myers Squibb, EMD Serono, GlaxoSmithKline, Impact Therapeutics, PrimeFour Therapeutics, Tango Therapeutics, Deerfield Management Company, Servier Bio-Innovation LLC, Covant Therapeutics, and Zentalis Pharmaceuticals; is an advisory board member for Impact Therapeutics; is a stockholder in Impact Therapeutics and PrimeFour Therapeutics; and reports receiving commercial research grants from Bristol Myers Squibb, EMD Serono, Moderna, and Tango Therapeutics. (Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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