J
Jennifer J. Young
Researcher at Massachusetts Institute of Technology
Publications - 5
Citations - 2666
Jennifer J. Young is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Senescence & DNA damage. The author has an hindex of 5, co-authored 5 publications receiving 2560 citations. Previous affiliations of Jennifer J. Young include University of California, San Francisco.
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miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis
Li Ma,Jennifer J. Young,Harsha K. Prabhala,Elizabeth Pan,Pieter Mestdagh,Daniel Muth,Julie Teruya-Feldstein,Ferenc Reinhardt,Tamer T. Onder,Scott Valastyan,Frank Westermann,Frank Speleman,Jo Vandesompele,Robert A. Weinberg +13 more
TL;DR: It is shown that miR-9, which is upregulated in breast cancer cells, directly targets CDH1, the E-cadherin-encoding messenger RNA, leading to increased cell motility and invasiveness, and a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis
miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis
Li Ma,Jennifer J. Young,Harsha K. Prabhala,Elizabeth Pan,Pieter Mestdagh,Daniel Muth,Julie Teruya-Feldstein,Ferenc Reinhardt,Tamer T. Onder,Scott Valastyan,Frank Westermann,Frank Speleman,Jo Vandesompele,Robert A. Weinberg +13 more
TL;DR: In this article, the authors uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasissuppressing protein E-cadherin.
Journal ArticleDOI
Continuous elimination of oxidized nucleotides is necessary to prevent rapid onset of cellular senescence
Priyamvada Rai,Tamer T. Onder,Jennifer J. Young,Jose L. McFaline,Bo Pang,Peter C. Dedon,Robert A. Weinberg +6 more
TL;DR: Results indicate that the nucleotide pool is a critical target of intracellular ROS and that oxidized nucleotides, unless continuously eliminated, can rapidly induce cell senescence through signaling pathways very similar to those activated during replicative senescences.
Journal ArticleDOI
Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence.
Priyamvada Rai,Jennifer J. Young,Jennifer J. Young,Dominick G. A. Burton,Maria G. Giribaldi,Tamer T. Onder,Tamer T. Onder,Robert A. Weinberg +7 more
TL;DR: It is demonstrated that overexpression of MTH1 can prevent the oncogenic H-RAS-induced DDR and attendant premature senescence, although it does not affect the observed elevation in ROS levels produced by RAS oncoprotein expression.
Journal ArticleDOI
Suppression of thioredoxin-1 induces premature senescence in normal human fibroblasts
TL;DR: It is found that suppression of TRX1 expression via shRNA rapidly induces premature senescence in young human skin fibroblasts through upregulation of the p53/p21(Cip1/Waf1) and p16(INK4a) tumor suppressor pathways.