Adi Dubash

Adi Dubash

Associate Professor of Biology

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Dr. Adi Dubash grew up in Mumbai, India. While always fascinated with Biology, his interest in an academic and scientific career was sparked by his work as an undergraduate research student, studying the behavior of breast cancer cells at The University of Texas at Austin. After graduating with a B.S. in Cell and Molecular Biology, he went on to complete a Ph.D. in Cell and Developmental Biology at The University of North Carolina at Chapel Hill. As a graduate student, his first author publication received the Best Paper of the Year Award from the Journal of Cell Science.

Continuing his research as a Postdoctoral Fellow at Northwestern University, Dr. Dubash’s work focused on understanding how attachment between cells is important for both normal tissue structure and onset of disease. Dr. Dubash’s postdoctoral tenure was strongly influenced by his involvement in mentoring students, and he is passionate about engaging undergraduates in rich and rewarding research experiences. At Furman University, Dr. Dubash has developed an undergraduate research training program aimed at providing students with a strong foundation in the scientific method, and experience in cutting-edge research to apply concepts learned from the classroom. Dr. Dubash's undergraduate research students have co-authored multiple publications and presented their research at international conferences such as the American Society for Cell Biology (ASCB)/European Molecular Biology Organization (EMBO) meetings.

Outside of work, Dr. Dubash enjoys opera, gardening, traveling and spending time with his husband and son.


  • Postdoctoral Fellow, Northwestern University
  • Ph.D., University of North Carolina at Chapel Hill
  • B.S., University of Texas at Austin


For any multicellular organism, attachment between cells is crucial for normal tissue function. These attachments (or adhesions) are made up of large complexes of proteins, which provide both the physical connection between cells (to form tissues) and signaling cues required for cells to survive, divide, migrate, and perform numerous other functions. Dr. Dubash's research investigates the mechanisms by which the desmosome adhesion complex controls normal tissue structure, and why defects in desmosome function contribute to a wide variety of pathologies, including cancer and heart disease.

To perform these studies, the Dubash lab employs the use of multiple cell culture models to grow lines of skin cancer, breast cancer, and cardiac muscle cells. Undergraduates in his lab use a variety of biochemical, molecular and cellular approaches to investigate the function of desmosomal proteins, such as transfections (to alter protein function), fluorescence microscopy (to image cell structure and behavior), western blotting (to analyze changes in protein levels and interactions), and quantitative PCR (to analyze changes in gene expression). To get an idea of what it is like to do research in the Dubash lab, please visit us on Instagram at dubashlab.


  • Shelton WT*, Thomas SM*, Alexander HR*, Thomes CE*, Conway DE, Dubash AD. (*undergraduate co-authors) (2021) Desmoglein-2 harnesses a PDZ-GEF2/Rap1 signaling axis to control spreading and focal adhesions independent of cell-cell adhesion. Scientific Reports, 11:13295.
  • Bendrick JL*, Eldredge LA*, Williams EI*, Haight NB*, Dubash AD. (*undergraduate co-authors) (2019) Desmoplakin Harnesses Rho GTPase and p38 Mitogen-Activated Protein Kinase Signaling to Coordinate Cellular Migration. Journal of Investigative Dermatology, 139(6):1227-1236.
  • Kam CY, Dubash AD, Magistrati E, Polo S, Satchell KJF, Sheikh F, Lampe P, Green KJ.(2018) Desmoplakin maintains gap junctions by inhibiting Ras/MAPK and lysosomal degradation of connexin-43. Journal of Cell Biology, 217(9):3219-35.
  • Dubash AD*, Kam CY*, Aguado, BA, Patel DM, Delmar M, Shea LD, Green KJ. (2016) (*co-first authors) Plakophilin-2 loss promotes TGF b1/p38 MAPK-dependent fibrotic gene expression in cardiomyocytes. Journal of Cell Biology, 212(4):425-38.
  • Albrecht LV, Green KJ, Dubash AD. (2016) The Cadherin Superfamily – Key Regulators of Animal Development and Physiology - Chapter 14: Cadherins in Cancer. Springer, ISBN: 978-4-431-56031-9.
  • Patel DM, Dubash AD, Kreitzer G, Green KJ. (2014) Desmoplakin (DP) mutations misregulate gap junctions by disrupting a novel DP-EB1 interaction. Journal of Cell Biology, 206(6):779-97.
  • Dubash AD, Koetsier JL, Harmon RH, Najor NA, Amargo EA, Green KJ. (2013) The GEF Bcr regulates Rho/MAL signaling in keratinocytes and differentiation via Desmoglein-1. Journal of Cell Biology, 202(4):653-66.
  • Guilluy C*, Dubash AD*, García-Mata R. (*co-first authors) (2011) Analysis of RhoA and Rho GEF activity in whole cells and the cell nucleus. Nature Protocols, 6(12):2050-60.
  • Dubash AD, Green KJ. (2011) Desmosomes. Current Biology, 21(14):R529-31.
  • Dubash AD*, Guilluy C*, Srougi MC, Boulter E, Burridge K, García-Mata R. (*co-first authors) (2011) RhoA activity in the nucleus is regulated by Net1 and is involved in the DNA damage response. PLoS One, 6(2):e17380.
  • Godsel LM, Dubash AD, Bass-Zubek AE, Amargo EV, Hobbs RP, Green KJ. (2010) Plakophilin 2 Couples Actomyosin Remodeling to Desmosomal Plaque Assembly via RhoA. Molecular Biology of the Cell, 21(16):2844-59.
  • García-Mata R, Dubash AD, Sharek L, Carr HS, Frost JA, Burridge K. (2007) The nuclear RhoA exchange factor Net1 interacts with proteins of the Dlg family, affects their localization, and influences their tumor suppressor activity. Molecular and Cellular Biology, 27(24):8683-97.
  • Dubash AD, Wennerberg K, García-Mata R, Menold MM, Arthur WT, Burridge K. (2007) A novel role for Lsc/p115 RhoGEF and LARG in regulating RhoA activity downstream of adhesion to fibronectin. Journal of Cell Science, 120(Pt 22):3989-98