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Jia-Ren Lin

Researcher at Harvard University

Publications -  55
Citations -  8431

Jia-Ren Lin is an academic researcher from Harvard University. The author has contributed to research in topics: Tumor microenvironment & Cell cycle. The author has an hindex of 23, co-authored 51 publications receiving 5029 citations. Previous affiliations of Jia-Ren Lin include National Taiwan University & Stanford University.

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An application of bioinformatics and text mining to the discovery of novel genes related to bone biology.

TL;DR: A text mining tool that analyzes the PubMed literature database and integrates the available genomic information to provide a detailed mapping of the genes and their interrelationships within a particular network such as osteoporosis shows that existing genomic data within the PubMed database can effectively be used to predict potentially novel target genes for osteop orosis research that have not previously been reported in the literature.
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DNA damage-specific deubiquitination regulates Rad18 functions to suppress mutagenesis.

TL;DR: Deubiquitination of Rad18 drives its localization to sites of DNA damage and formation of the Rad18–SHPRH complexes necessary for error-free lesion bypass.
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Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma.

Pratiti Bandopadhayay, +89 more
TL;DR: Both the response and resistance to BET inhibitors in mice is mediated by bHLH/homeobox transcription factors, which provides insights about the mechanisms underlying BETi effects and the appearance of resistance and support the therapeutic use of combined cell-cycle inhibitors with BETi in MYC-amplified medulloblastoma.
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Small-Molecule Screen Identifies De Novo Nucleotide Synthesis as a Vulnerability of Cells Lacking SIRT3

TL;DR: A metabolic vulnerability of cells with Sirtuin 3 loss is uncovered by using an unbiased small-molecule screen and it is found that SIRT3 KO cells upregulated the diversion of glutamine into de novo nucleotide synthesis through hyperactive mTORC1 signaling.
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Determinants of drug-target interactions at the single cell level.

TL;DR: It is demonstrated that non-specific interactions lead to very slow incorporation kinetics of DNA binding drugs, which leads to virtually irreversible binding of the drug to specific DNA targets in cells.