Tanya Freedman, PhD
Assistant Professor, Department of Pharmacology

Contact Info
Assistant Professor, Department of Pharmacology
Faculty, Microbiology, Immunology and Cancer Biology (MICaB) Ph.D. Graduate Program
Faculty, MS and PhD Programs in Molecular Pharmacology and Therapeutics (MPaT)
Faculty, PhD Program in Biochemistry, Molecular Biology and Biophysics
Preceptor, Medical Scientist Training Program (Combined MD/PhD Training Program)
Postdoctoral Fellowship, University of California, San Francisco
PhD, University of California, Berkeley, Molecular and Cell Biology
AB, Bowdoin College, Brunswick, ME, Biochemistry
Summary
Dr. Freedman is an Assistant Professor of Pharmacology, housed in the Center for Immunology at University of Minnesota (UMN). She is also a member of the UMN Masonic Cancer Center's Immunology Program and the Center for Autoimmune Diseases Research. She received her AB degree with honors in Biochemistry from Bowdoin College (Brunswick, ME) before moving to UC Berkeley to enter the PhD program in Molecular and Cell Biology. Working jointly in the laboratories of Drs. John Kuriyan and Susan Marqusee, Dr. Freedman discovered structural and dynamic mechanisms underlying differential allosteric activation of the Ras-activating proteins Sos and RasGRF1. As a postdoc with Dr. Arthur Weiss at UCSF, she discovered a mechanism by which the Src-family kinase LynA tunes macrophage sensitivity to pro-inflammatory activation, a process with implications for myeloid-cell hypersensitization in autoimmune disease. Dr. Freedman's independent research program at UMN focuses on how myeloid cells integrate positive- and negative-regulatory signals to achieve tissue-specific functions and drive pathologies from autoimmune diseases to breast cancer. Protein tyrosine kinases, including Lyn and the other Src-family kinases, are modulators of cell sensitivity, and thus cell- and receptor-specific modes of kinase regulation and function are areas of special interest to her lab.
Expertise
Immunology
Innate-immune signaling
Cancer immune microenvironment
Autoimmune disease
Biochemistry
Awards & Recognition
NIH T32 Training Award (Predoctoral Student Monica Sauer) CA009138 (2021) American Cancer Society – Kirby Foundation Postdoctoral Fellowship (J.T. Greene) PF-21-068-01-LIB (2021) NIH R01 Grant AR073966 (2018) Travel Award, FASEB Science Research Conferences (2018) Travel Award, FASEB Science Research Conferences (2017) NIH R03 Grant AI130978 (2017) NIH T32 Training Award (Predoctoral Student Ben Brian) DA007097 (2016) NIH F32 NRSA Individual Postdoctoral Fellowship F32 AI082926 (2011) Outstanding Graduate Student Instructor Award, University of California, Berkeley (2004) Copeland-Gross Biology Prize, Bowdoin College, Brunswick, ME (1999) Howard Hughes Medical Institute REU Fellowship (1998) NIH T32 Training Award (Postdoctoral Fellow J.T. Greene) CA009138 (2020) Dr. Marvin and Hadassah Bacaner Research Award in Pharmacology (Predoctoral Student Ben Brian), UMN Medical School (2020) Frederick E. Shideman Research Proposal Award (Predoctoral Student Ben Brian), Department of Pharmacology (2019) J. Jacob Kaplan Award in Clinical or Basic Medical Research (Predoctoral Student Ben Brian), UMN Medical School (2020) Veneziale-Steer Award for Research in Cellular Growth Regulation (Predoctoral Student Ben Brian), UMN Medical School (2020)
Professional Associations
American College of Rheumatology (ACR) The American Association of Immunologists (AAI) American Association for Cancer Research (AACR)
Research
Research Summary/Interests
Immune cells are tuned exquisitely to identify pathogens and avoid hypersensitivity. In macrophages Src-family tyrosine kinases (LynA, LynB, Hck, and Fgr) regulate a size sensing mechanism based on their ability to nucleate clustering of ITAM-coupled receptors. Under normal circumstances small debris cannot trigger macrophage activation, but this regulatory process can be subverted in inflamed tissues. We are studying how the Src-family kinases, especially LynA, tune the sensitivity of macrophages and other immune cells to triggering and the regulation or dysregulation of these processes in autoimmune disease, infection, and breast cancer.