Mallar Bhattacharya Medicine, UCSF, San Francisco
1 protocol

  • Postdoctoral Fellow, Boston University, 2016
Research focus
  • Immunology
  • 1 Author merit


Postdoctoral Fellow, Livestrong Cancer Institute, UT Austin, USA, 2019

• Aran, D., Looney, A. P., Liu, L., Wu, E., Fong, V., Hsu, A., Chak, S., Naikawadi, R. P., Wolters, P. J., Abate, A. R., Butte, A. J. and Bhattacharya, M. (2019). Reference-based analysis of lung single-cell sequencing reveals a transitional profibrotic macrophage. Nat Immunol 20(2): 163-172.
• Fong, V., Hsu, A., Wu, E., Looney, A. P., Ganesan, P., Ren, X., Sheppard, D., Wicher, S. A., Thompson, M. A., Britt, R. D., Jr., Prakash, Y. S. and Bhattacharya, M. (2018). Arhgef12 drives IL17A-induced airway contractility and airway hyperresponsiveness in mice. JCI Insight 3(21).
• Toyama, T., Looney, A. P., Baker, B. M., Stawski, L., Haines, P., Simms, R., Szymaniak, A. D., Varelas, X. and Trojanowska, M. (2018). Therapeutic Targeting of TAZ and YAP by Dimethyl Fumarate in Systemic Sclerosis Fibrosis. J Invest Dermatol 138(1): 78-88.
• Grzegorzewska, A. P., Seta, F., Han, R., Czajka, C. A., Makino, K., Stawski, L., Isenberg, J. S., Browning, J. L. and Trojanowska, M. (2017). Dimethyl Fumarate ameliorates pulmonary arterial hypertension and lung fibrosis by targeting multiple pathways. Sci Rep 7: 41605.
• Looney, A. P., Han, R., Stawski, L., Marden, G., Iwamoto, M. and Trojanowska, M. (2017). Synergistic Role of Endothelial ERG and FLI1 in Mediating Pulmonary Vascular Homeostasis. Am J Respir Cell Mol Biol 57(1): 121-131.
• Bohnert, K. A., Grzegorzewska, A. P., Willet, A. H., Vander Kooi, C. W., Kovar, D. R. and Gould, K. L. (2013). SIN-dependent phosphoinhibition of formin multimerization controls fission yeast cytokinesis. Genes Dev 27(19): 2164-2177.
1 Protocol published
Authors:  Agnieszka P. Looney and Mallar Bhattacharya, date: 08/20/2019, view: 3219, Q&A: 0
Pulmonary fibrosis is characterized by pathological scaring of the lung. Similar to other fibrotic diseases, scar formation is driven by excessive extracellular matrix deposition by activated, proliferative, and migratory fibroblasts.

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