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Identification and Characterization of TPRKB Dependency in TP53 Deficient Cancers

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서명/저자사항Identification and Characterization of TPRKB Dependency in TP53 Deficient Cancers.
개인저자Kennaley, Kelly.
단체저자명University of Michigan. Molecular & Cellular Pathology.
발행사항[S.l.]: University of Michigan., 2019.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2019.
형태사항171 p.
기본자료 저록Dissertations Abstracts International 81-06B.
Dissertation Abstract International
ISBN9781392870372
학위논문주기Thesis (Ph.D.)--University of Michigan, 2019.
일반주기 Source: Dissertations Abstracts International, Volume: 81-06, Section: B.
Advisor: Nikolovska-Coleska, Zaneta
이용제한사항This item must not be sold to any third party vendors.This item must not be added to any third party search indexes.
요약Tumor protein 53 (TP53) is a transcription factor involved in regulating various facets of cellular functionality from its canonical functions in DNA damage response, cell cycle arrest, and apoptosis, to newer roles in metabolism, protein translation, and more. TP53 is also the most frequently altered gene in human cancer, and identification of vulnerabilities imposed by TP53 alterations may enable development of effective therapeutic approaches. Through analyzing shRNA-screening data, we identified TP53RK binding protein (TPRKB) as the most significant vulnerability in TP53-mutated cancer cell lines. To date, TPRKB's only known role is as a poorly characterized member of the transfer RNA (tRNA)-modifying Endopeptidase-like and Kinase associated to transcribed Chromatin/Kinase, Endopeptidase and Other Proteins of small Size (EKC/KEOPS) complex, responsible for depositing the t6A37 modification on all ANN decoding tRNAs. In vitro and in vivo, across multiple benign-immortalized and cancer cell lines, we confirmed that TPRKB knockdown in TP53-null, TP53-mutated, and Mouse double minute 2 homolog (MDM2
일반주제명Cellular biology.
Biology.
Molecular biology.
언어영어
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