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Deng, Lin

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Deng

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Deng, Lin

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Now showing 1 - 4 of 4
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    Publication
    Metabolic Syndrome, Inflammation, and Cancer
    (Hindawi, 2017) Wu, Yong; Dong, Yunzhou; Duan, Shengzhong; Zhu, Donghui; Deng, Lin
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    Corrigendum to “Metabolic Syndrome, Inflammation, and Cancer”
    (Hindawi, 2017) Wu, Yong; Dong, Yunzhou; Duan, Shengzhong; Zhu, Donghui; Deng, Lin
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    Publication
    On the unsupervised analysis of domain-specific Chinese texts
    (Proceedings of the National Academy of Sciences, 2016) Deng, Lin; Bol, Peter; Li, Kate J.; Liu, Jun
    With the growing availability of digitized text data both publicly and privately, there is a great need for effective computational tools to automatically extract information from texts. Because the Chinese language differs most significantly from alphabet-based languages in not specifying word boundaries, most existing Chinese text-mining methods require a prespecified vocabulary and/or a large relevant training corpus, which may not be available in some applications. We introduce an unsupervised method, top-down word discovery and segmentation (TopWORDS), for simultaneously discovering and segmenting words and phrases from large volumes of unstructured Chinese texts, and propose ways to order discovered words and conduct higher-level context analyses. TopWORDS is particularly useful for mining online and domain-specific texts where the underlying vocabulary is unknown or the texts of interest differ significantly from available training corpora. When outputs from TopWORDS are fed into context analysis tools such as topic modeling, word embedding, and association pattern finding, the results are as good as or better than that from using outputs of a supervised segmentation method.
  • Publication
    TRAIP is a master regulator of DNA interstrand crosslink repair
    (Springer Nature, 2019-03) Wu, Alexander; Semlow, Daniel; Kamimae-Lanning, Ashley N.; Kochenova, Olga; Chistol, Gheorghe; Hodskinson, Michael R.; Amunugama, Ravindra; Sparks, Justin; Wang, Meng; Deng, Lin; Mimoso, Claudia; Low, Emily; Patel, Ketan J.; Walter, Johannes
    Cells often utilize multiple pathways to repair the same DNA lesion, and pathway choice has profound implications for the fidelity of genome maintenance. DNA interstrand cross-links (ICLs) block DNA replication and transcription by covalently linking the two strands of DNA, and the cytotoxicity of ICLs is exploited for chemotherapy. In Xenopus egg extracts, replication fork collision with ICLs initiates two distinct repair pathways. The NEIL3 glycosylase can cleave the cross-link1, but if this fails, the Fanconi anemia (FA) proteins incise the phosphodiester backbone surrounding the ICL, generating a double-strand break (DSB) intermediate that is repaired by homologous recombination2. How the simpler NEIL3 pathway is prioritized over the FA pathway, which can cause genomic rearrangements, is unknown. Here, we show that the E3 ubiquitin ligase TRAIP regulates both pathways. TRAIP appears to associate with the leading edge of the replisome, ubiquitylating any protein in the replisome’s path, including the replicative DNA helicase CMG (CDC45-MCM2-7-GINS) when two replisomes converge at an ICL. In this setting, short ubiquitin chains recruit NEIL3 through direct binding, whereas longer chains are required for CMG unloading by the p97 ATPase, enabling the FA pathway. Our results identify TRAIP as a master regulator of replisome stability and ICL repair pathway choice.