Sasha Shafikhani, Ph.D.

Sasha Shafikhani, PhD

Research/Academic Interests

As a cellular microbiologist, Shafikhani's research strategy involves leveraging insights from pathogen studies to enhance the understanding of host cellular processes. His lab primarily focuses on identifying the virulence mechanisms that drive Pseudomonas aeruginosa pathogenesis in wound infections, as well as investigating the eukaryotic host responses aimed at controlling these infections. Additionally, Shafikhani's team uses bacterial toxins as molecular tools to explore critical mammalian cellular processes, including cytokinesis, apoptotic programmed cell death, and apoptotic compensatory proliferation signaling. Recent projects in the lab are centered on identifying the dysfunctional mechanisms that make diabetic wounds susceptible to infection and impair their healing processes.

Title: Professor & Director of Microbiome Research

Undergraduate Education: University of California Berkeley, Berkeley, California, B.A., Molecular Cell Biology, 1991

Graduate Education: University of California Berkeley, Berkeley, California, Ph.D., Mircobiology, 2001

Fellowship: University of California San Francisco, San Francisco, California, Infections Diseases, 2008

Professional Memberships

Wound Healing Society

American Society for Microbiology

American Society for Cell Biology

Selected Recent Peer-reviewed Publications:

For all publications, click here.

Ruchi Roy, Foyez Mahmud, Janet Zayas, Timothy M. Kuzel, Jochen Reiser, & Sasha H. Shafikhani. Reduced Bioactive Microbial Products (PAMPs) Contribute to Dysregulated Immune Responses And Impaired Healing in Infected Wounds in Diabetic Mice. Journal of Investigative Dermatology. 2024, Feb;144(2):387-397.e11. PMID: 37619833. PMCID: PMC10840742; DOI: https://doi.org/10.1016/j.jid.2023.08.004.

- Mohamed F. Mohamed, Kajal Gupta, Josef W. Goldufsky, Ruchi Roy, Lauren T. Callaghan, Dawn M. Wetzel, Timothy M. Kuzel, Jochen Reiser & Sasha H. Shafikhani. CrkII/Abl phosphorylation cascade is critical for NLRC4 inflammasome activity and is blocked by Pseudomonas ExoT. Nature Communications. 2022 Mar 11. 13(1):1295. doi: 10.1038/s41467-022-28967-5. PMID: 35277504. PMCID: PMC8917168.

Ruchi Roy, Janet Zayas, Sunil K. Singh, Kaylee Delgado, Stephen J. Wood, Mohamed F. Mohamed, Dulce M. Frausto, Yasmeen A. Albalawi, Thea P. Price, Ricardo Estupinian , Eileena F. Giurini, Timothy M. Kuzel, Andrew Zloza, Jochen Reiser, & Sasha H Shafikhani. Overriding impaired FPR chemotaxis signaling in diabetic neutrophil stimulates infection control in murine diabetic wound. eLife. 2022, Feb 3. 11:e72071. doi: 10.7554/eLife.72071. PMID: 35112667. PMCID: PMC8846594.

Ruchi Roy, Janet Zayas, Mohamed F. Mohamed, Mohammad Bayat, Timothy M. Kuzel, Jochen Reiser & Sasha H. Shafikhani. IL-10 Dysregulation underlies Global Chemokine Insufficiency, Delayed Macrophage Response, and Impaired Healing in Diabetic Wound. Journal of Investigative Dermatology. 2022 Mar. 142(3 Pt A):692-704.e14. doi: 10.1016/j.jid.2021.08.428. Epub 2021 Sep 10. PMID: 34517005. PMCID: PMC8860852.

Kajal H. Gupta, Josef W. Goldufsky, Stephen J. Wood, Nicholas J. Tardi, Gayathri S. Moorthy, Douglas Z. Gilbert, Janet P. Zayas, Eunsil Hahm, Mehmet M. Altintas, Jochen Reiser, & Sasha H. Shafikhani. Apoptosis and compensatory proliferation signaling are coupled by CrkI-containing microvesicles. Developmental Cell. 2017, Jun 19. 41(6):674-684.e5. PMID: 28633020, PMCID: PMC5533184. doi: 10.1016/j.devcel.2017.05.014.

Call Us fora MedicalDermatologyAppointment916-734-6111

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Dermatology
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