{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":[null],"species":["Homo sapiens (human) and Saccharomyces cerevisiae"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-BSST1043"],"repository":["biostudies-other"],"additional_accession":["A Sterol-PI(4)P exchanger controls the Tel1/ATM axis of the DNA Damage Response"]},"is_claimable":false,"name":"A Sterol-PI(4)P exchanger controls the Tel1/ATM axis of the DNA Damage Response\n","description":"Source blots, micrographs and numerical values for the aforementioned study, whose abstract is: \"Upon DNA damage, cells activate the DNA Damage Response (DDR) to coordinate proliferation and DNA repair. Dietary, metabolic, and environmental inputs are emerging as modulators of how DNA surveillance and repair take place. Lipids hold potential to convey these cues, although little is known about how. We observed that lipid droplet (LD) number specifically increased in response to DNA breaks. We show that the selective storage of sterols into these LD concomitantly stabilizes phosphatidyl-4-inositol (PI(4)P) at the Golgi, where it binds the DDR kinase ATM. In turn, this titration attenuates the initial nuclear ATM-driven response to DNA breaks, thus allowing processive repair. Further, manipu","dates":{"release":"2023-03-05T00:00:00Z","modification":"2023-03-02T13:31:22.625Z","creation":"2023-03-02T13:31:22.625Z"},"accession":"S-BSST1043","cross_references":{"biostudies":["A Sterol-PI(4)P exchanger controls the Tel1/ATM axis of the DNA Damage Response"]}}