Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/148503
Title: T-ALL ASSOCIATED NAP1L1-MLLT10 FUSION PROTEIN PROMOTES TELOMERASE-MEDIATED TELOMRERE ELONGATION
Authors: WANG JING
Keywords: Telomere,Telomerase,T-cell acute lymphoblastic leukemia ,NAP1L1-MLLT10,Telomere elongation,Telomerase-associated protein
Issue Date: 19-Jun-2018
Citation: WANG JING (2018-06-19). T-ALL ASSOCIATED NAP1L1-MLLT10 FUSION PROTEIN PROMOTES TELOMERASE-MEDIATED TELOMRERE ELONGATION. ScholarBank@NUS Repository.
Abstract: Telomere length elongation is an essential physiological process in cancer cells. The telomerase counteracts telomere attrition. Cell cycle-dependent regulation of telomerase recruitment to telomeres is not only critical for maintaining telomere length equilibrium, but also for its coupling with DNA replication. However, the molecular mechanisms underlying the cell cycle-dependent telomerase recruitment to telomeres are only partially understood. Here we have identified nucleosome assembly protein 1-like1 (NAP1L1) as a novel TERT- associated protein. Our data indicates that NAP1L1 interacts with TERT and TRF1 through distinct functional domains and promotes telomerase-mediated telomere elongation. NAP1L1 is highly expressed in T-ALL cell lines, and recurrent NAP1L1-MLLT10 fusions have been reported in T-ALL patients. Our data indicates that overexpression of NAP1L1- MLLT10 fusion protein promotes telomere maintenance in cancer cells. These results provide new insights into the mechanisms of telomere maintenance as well as potential strategies for therapeutic intervention of T-ALL with NAP1L1- MLLT10 fusion.
URI: http://scholarbank.nus.edu.sg/handle/10635/148503
Appears in Collections:Ph.D Theses (Open)

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