Xin Gu, PhD

Xin Gu, PhD

Contact Information

Office Phone Number

(617) 632-4594

Biography

Xin Gu, PhD

Dr. Gu started her lab as an independent investigator at DFCI and an assistant professor of Cell Biology at Harvard Medical School in September 2024. She received her BS in Biology from Peking University, and her PhD in Biology from Massachusetts Institute of Technology, where she studied mechanism of nutrient sensing upstream of mTORC1. She conducted postdoctoral research on ubiquitin-independent protein degradation mechanisms in the Department of Neurobiology at Harvard Medical School. She is a recipient of a Damon Runyon postdoctoral fellowship, the David H. Hubel outstanding postdoctoral fellow award (Department of Neurobiology, HMS), and an Aramont Fellowship Fund for Emerging Science Research (HMS).

Researcher

Physician

Assistant Professor of Cell Biology, Harvard Medical School
Assistant Professor of Cancer Biology, Dana-Farber Cancer Institute

Fellowship

  • Aramont Fellowship Fund for Emerging Science Research: Harvard Medical School
  • Damon Runyon postdoctoral fellowship: Harvard Medical School, Dept of Neurobiology

Recent Awards

  • Damon Runyon postdoctoral fellowship
  • The David H. Hubel outstanding postdoctoral fellow award (Department of Neurobiology, HMS
  • An Aramont Fellowship Fund for Emerging Science Research (HMS)

Research

    Unveiling the crosstalk between protein turnover and transcription

    The Gu Lab focuses on elucidating how cells regulate proteasomal degradation independently of ubiquitination. We discovered a non-canonical proteolysis mechanism, the midnolin-proteasome pathway, that bypasses ubiquitination to selectively degrade numerous stimulus-responsive and cell-type specific transcription factors including EGR1, IRF4, Fos, NeuroD1, STAT3, and NR4A1. The Gu lab will characterize the midnolin-proteasome pathway using biochemical, structural, and cellular experiments. Additionally, genetically engineered animal models will be used to determine the roles of midnolin in organismal physiology and pathology. The long-term goal is to manipulate the midnolin-proteasome pathway either genetically or pharmacologically to control brain functions, modulate the immune system, and destroy cancer cells. The Gu lab is also interested in identifying other ubiquitin-independent mechanisms that degrade different substrate repertoires as well as the crosstalk of protein homeostasis with chromatin biology and metabolism. Overall, we seek to elucidate fundamental mechanisms related to cell biology using a diverse experimental tool kit.

    Research Departments

    Publications

      • Rag-Ragulator is the central organizer of the physical architecture of the mTORC1 nutrient-sensing pathway. Proc Natl Acad Sci U S A. 2024 Aug 27; 121(35):e2322755121. View in: Pubmed

      • The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation. Science. 2023 08 25; 381(6660):eadh5021. View in: Pubmed

      • A central role for regulated protein stability in the control of TFE3 and MITF by nutrients. Mol Cell. 2023 01 05; 83(1):57-73.e9. View in: Pubmed

      • Author Correction: Sestrin mediates detection of and adaptation to low-leucine diets in Drosophila. Nature. 2022 Sep; 609(7929):E11. View in: Pubmed

      • Sestrin mediates detection of and adaptation to low-leucine diets in Drosophila. Nature. 2022 08; 608(7921):209-216. View in: Pubmed

      • Structure of the nutrient-sensing hub GATOR2. Nature. 2022 07; 607(7919):610-616. View in: Pubmed

      • Structural basis for the docking of mTORC1 on the lysosomal surface. Science. 2019 10 25; 366(6464):468-475. View in: Pubmed

      • Arg-78 of Nprl2 catalyzes GATOR1-stimulated GTP hydrolysis by the Rag GTPases. J Biol Chem. 2019 02 22; 294(8):2970-2975. View in: Pubmed

      • SAMTOR is an S-adenosylmethionine sensor for the mTORC1 pathway. Science. 2017 11 10; 358(6364):813-818. View in: Pubmed

      • KICSTOR recruits GATOR1 to the lysosome and is necessary for nutrients to regulate mTORC1. Nature. 2017 03 16; 543(7645):438-442. View in: Pubmed

      Locations

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      Longwood Center

      360 Brookline Ave Longwood Center LC6312 Boston, MA 02215
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      Longwood Center

      Location Avtar

      Longwood Center

      360 Brookline Ave Longwood Center LC6312 Boston, MA 02215
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      42.3386, -71.1073

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