Honors & Awards

  • Predoctoral Fellowship, Ford Foundation (2022-2025)
  • Stanford Interdisciplinary Graduate Fellowship (SIGF), Stanford VPGE (2022-2025)
  • Gates Millennium Scholar, Bill and Melinda Gates Foundation (2016–2024)

Education & Certifications

  • B.S. (Hons), University of Chicago, Biological Sciences (2020)

Contact

  • Academic
    gbarron@stanford.edu
    University - Student Department: School of Medicine - IDP's - Immunology Position: Graduate

Additional Info

Research Interests

  • Equity in Education
  • Research Methods
  • Science Education

Lab Affiliations

All Publications

  • Gut microbiota modulate susceptibility to bleomycin-induced lung injury Yoon, Y., Barron, G. M., Hrusch, C. L., Fei, N., Leone, V. A., Sperling, A. I. AMER ASSOC IMMUNOLOGISTS. 2021

    View details for Web of Science ID 000713665801316

  • P311 Promotes Lung Fibrosis via Stimulation of Transforming Growth Factor-β1, -β2, and -β3 Translation. American journal of respiratory cell and molecular biology Duan, F. F., Barron, G., Meliton, A., Mutlu, G. M., Dulin, N. O., Schuger, L. 2019; 60 (2): 221-231

    Abstract

    Interstitial lung fibrosis, a frequently idiopathic and fatal disease, has been linked to the increased expression of profibrotic transforming growth factor (TGF)-βs. P311 is an RNA-binding protein that stimulates TGF-β1, -β2, and -β3 translation in several cell types through its interaction with the eukaryotic translation initiation factor 3b. We report that P311 is switched on in the lungs of patients with idiopathic pulmonary fibrosis (IPF) and in the mouse model of bleomycin (BLM)-induced pulmonary fibrosis. To assess the in vivo role of P311 in lung fibrosis, BLM was instilled into the lungs of P311-knockout mice, in which fibrotic changes were significantly decreased in tandem with a reduction in TGF-β1, -β2, and -β3 concentration/activity compared with BLM-treated wild-type mice. Complementing these findings, forced P311 expression increased TGF-β concentration/activity in mouse and human lung fibroblasts, thereby leading to an activated phenotype with increased collagen production, as seen in IPF. Consistent with a specific effect of P311 on TGF-β translation, TGF-β1-, -β2-, and -β3-neutralizing antibodies downregulated P311-induced collagen production by lung fibroblasts. Furthermore, treatment of BLM-exposed P311 knockouts with recombinant TGF-β1, -β2, and -β3 induced pulmonary fibrosis to a degree similar to that found in BLM-treated wild-type mice. These studies demonstrate the essential function of P311 in TGF-β-mediated lung fibrosis. Targeting P311 could prove efficacious in ameliorating the severity of IPF while circumventing the development of autoimmune complications and toxicities associated with the use of global TGF-β inhibitors.

    View details for DOI 10.1165/rcmb.2018-0028OC

    View details for PubMedID 30230348

    View details for PubMedCentralID PMC6376409

https://orcid.org/0000-0002-1442-5072