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Jin Ying Shao on Muck Rack

Jin Ying Shao

As seen in: Nature, Wiley Online Library, MDPI, Royal Society of Chemistry, Cell Press, BiggerPockets, American Society for Microbiology (ASM)
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Articles

TET2 loss triggers ssDNA gap accumulation and heightened PARP inhibitor sensitivity

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By Sumedha Agashe, William Jacobs, Vladislav O. Sviderskiy, Celia D. Rouault, Yixuan Xie, Carolina Brás-Costa, Emily Zahn, Mary Claire Kendall, Alice Meroni, Matthew Wood, Barbara Soares, Jin Ying Shao, Maggie Cox, Grant A. Challen, John J. Krais, Matthew Walter, Stephen T. Oh, Benjamin Garcia, John Edwards, Priyanka Verma, Alessandro Vindigni, Nidhi Athreya, Christopher T. Letson
| Nature Verified
Abstract Somatic mutations in the de novo methyltransferase DNMT3A and cytosine demethylase TET2 are common in age-related clonal hematopoiesis and hematopoietic neoplasms. TET2 mutations, unlike DNMT3A mutations, increase sensitivity to PARP inhibitors (PARPi). We find that TET2 loss, but not DNMT3A loss, alters DNA replication fork progression upon treatment with PARPi Olaparib, resulting in longer DNA replication tracts and increased DNA breaks.
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Impact of Changjiang-Hanjiang Water Diversion Project on the runoff process in the lower reach of Hanjiang River

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By Jin Ying Shao, Yuxin Zhang, Jiming Jin, Taohua He, Qian Luo, Yuan Zhou, Yun Kong, Chuan Liang
| Nature Verified
Abstract Inter-basin water transfer is a commonly adopted measure for improving hydrological and ecological conditions within watersheds. However, systematically quantifying the actual improvement effects of water diversion projects on watershed runoff conditions remains a weak link in current hydraulic engineering evaluation.
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U2af1 S34F and U2af1 Q157R myeloid neoplasm-associated hotspot mutations induce distinct hematopoietic phenotypes in mice

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By Michael O. Alberti, Sridhar Nonavinkere Srivatsan, Jin Ying Shao, Dennis L. Fei, Mengou Zhu, Monique Chavez, Stefan P. Tarnawsky, Sarah Grieb, Timothy A Graubert, Omar Abdel-Wahab Verified, Matthew Walter, Claudia Cabrera Pastrana
| Nature Verified
Abstract Recurrent somatic mutations in the spliceosome genes SF3B1, SRSF2, and U2AF1 are frequently identified in patients with myeloid neoplasms, such as myelodysplastic syndromes. We characterized the in vivo consequences of expressing two hotspot mutations in U2AF1 that code for the S34F and Q157R substitutions.
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