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Nan Yan
Researcher at University of Texas Southwestern Medical Center
Publications - 57
Citations - 6221
Nan Yan is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Innate immune system & Sting. The author has an hindex of 27, co-authored 46 publications receiving 5060 citations. Previous affiliations of Nan Yan include Boston Children's Hospital & Harvard University.
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Journal ArticleDOI
Identification of Host Proteins Required for HIV Infection Through a Functional Genomic Screen
Abraham L. Brass,Derek M. Dykxhoorn,Yair Benita,Nan Yan,Alan Engelman,Ramnik J. Xavier,Judy Lieberman,Stephen J. Elledge +7 more
TL;DR: This article performed a large-scale small interfering RNA screen to identify host factors required by HIV-1 and identified more than 250 HIV-dependency factors (HDFs), which participate in a broad array of cellular functions and implicate new pathways in the viral life cycle.
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Cyclic GMP-AMP Synthase Is an Innate Immune Sensor of HIV and Other Retroviruses
Daxing Gao,Jiaxi Wu,You Tong Wu,Fenghe Du,Chukwuemika Aroh,Nan Yan,Lijun Sun,Zhijian J. Chen +7 more
TL;DR: Results indicate that cGAS is an innate immune sensor of HIV and other retroviruses, suggesting that the reverse-transcribed HIV DNA triggers the innate immune response.
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miR-24 Inhibits Cell Proliferation by Targeting E2F2, MYC, and Other Cell-Cycle Genes via Binding to “Seedless” 3′UTR MicroRNA Recognition Elements
Ashish Lal,Francisco Navarro,Christopher G. Maher,Laura E. Maliszewski,Nan Yan,Elizabeth M. O'Day,Dipanjan Chowdhury,Derek M. Dykxhoorn,Derek M. Dykxhoorn,Perry Tsai,Oliver Hofmann,Kevin G. Becker,Myriam Gorospe,Winston Hide,Winston Hide,Judy Lieberman +15 more
TL;DR: MiR-24, upregulated during terminal differentiation of multiple lineages, inhibits cell-cycle progression and regulates expression of E2F2, MYC, AURKB, CCNA2, CDC2, CDK4, and FEN1 by recognizing seedless but highly complementary sequences.
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The cytosolic exonuclease TREX1 inhibits the innate immune response to human immunodeficiency virus type 1
TL;DR: Trex1 bound to cytosolic HIV DNA and digested excess HIV DNA that would otherwise activate interferon expression via a pathway dependent on the kinase TBK1, the adaptor STING and the transcription factor IRF3, finding that HIV-stimulated interferons production in cells deficient in TREX1 did not involve known nucleic acid sensors.
Journal ArticleDOI
Intrinsic antiviral immunity
Nan Yan,Zhijian J. Chen +1 more
TL;DR: This review focuses on recent advances in understanding of the roles of intrinsic antiviral factors that restrict infection by human immunodeficiency virus and influenza virus.