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dc.contributor.authorCrighton, Den_US
dc.contributor.authorWilkinson, Sen_US
dc.contributor.authorO Prey, Jen_US
dc.contributor.authorSyed, Nen_US
dc.contributor.authorSmith, Pen_US
dc.contributor.authorHarrison, PRen_US
dc.contributor.authorGasco, Men_US
dc.contributor.authorGarrone, Oen_US
dc.contributor.authorCrook, Ten_US
dc.contributor.authorRyan, KMen_US
dc.date.accessioned2018-09-03T13:02:47Z
dc.date.issued2006-07-14en_US
dc.identifier1en_US
dc.identifier.citationCELL, 2006, 126 pp. 121 - 134en_US
dc.identifier.issn0092-8674en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2508
dc.identifier.doi10.1016/j.cell.2006.05.034en_US
dc.description.abstractInactivation of cell death is a major step in tumor development, and p53, a tumor suppressor frequently mutated in cancer, is a critical mediator of cell death. While a role for p53 in apoptosis is well established, direct links to other pathways controlling cell death are unknown. Here we describe DRAM (damage-regulated autophagy modulator), a p53 target gene encoding a lysosomal protein that induces macroautophagy, as an effector of p53-mediated death. We show that p53 induces autophagy in a DRAM-dependent manner and, while overexpression of DRAM alone causes minimal cell death, DRAM is essential for p53-mediated apoptosis. Moreover, analysis of DRAM in primary tumors revealed frequent decreased expression often accompanied by retention of wildtype p53. Collectively therefore, these studies not only report a stress-induced regulator of autophagy but also highlight the relationship of DRAM and autophagy to p53 function and damage-induced programmed cell death.en_US
dc.format.extent121 - 134en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherCELL PRESSen_US
dc.titleDRAM, a p53-induced modulator of autophagy, is critical for apoptosisen_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1016/j.cell.2006.05.034en_US
rioxxterms.licenseref.startdate2006-07-14en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfCELLen_US
pubs.notesaffiliation: Ryan, KM (Reprint Author), Beatson Inst Canc Res, Canc Res UK Beatson Labs, Tumour Cell Death Lab, Garscube Estate,Switchback Rd, Glasgow G61 1BD, Lanark, Scotland. Beatson Inst Canc Res, Canc Res UK Beatson Labs, Tumour Cell Death Lab, Glasgow G61 1BD, Lanark, Scotland. Beatson Inst Canc Res, Canc Res UK Beatson Labs, Oral Canc Mol Genet Lab, Glasgow G61 1BD, Lanark, Scotland. Inst Canc Res, Chester Beatty Labs, Breakthrough toby Robins Breast Canc Res Ctr, London SW3 6JB, England. Osped San Croce & Carle, Dept Med Oncol, Cuneo, Italy. keywords-plus: PROGRAMMED CELL-DEATH; DNA-DAMAGE; IN-VIVO; GENE; P53; CANCER; PROTEINS; INACTIVATION; ASSOCIATION; DEGRADATION research-areas: Biochemistry & Molecular Biology; Cell Biology web-of-science-categories: Biochemistry & Molecular Biology; Cell Biology author-email: k.ryan@beatson.gla.ac.uk orcid-numbers: Ryan, Kevin M./0000-0002-1059-9681 Wilkinson, Simon/0000-0003-1082-8218 number-of-cited-references: 41 times-cited: 755 usage-count-last-180-days: 2 usage-count-since-2013: 55 journal-iso: Cell doc-delivery-number: 066JF unique-id: ISI:000239224800021 oa: gold_or_bronze da: 2018-09-03en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.volume126en_US
pubs.embargo.termsNot knownen_US
dc.contributor.icrauthorSmith, Paulen_US
dc.contributor.icrauthorCrook, Timothyen_US
dc.contributor.icrauthorSyed, Neloferen_US


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