Embedded Files
Selected Publications
CrkII/Abl phosphorylation cascade is critical for NLRC4 inflammasome activity and is blocked by Pseudomonas aeruginosa ExoT. Nature Communications, 2022
This research reveals how a bacterial virulence factor can disrupt a critical host immune pathway. Understanding this host–pathogen interaction provides new insight into bacterial infection and may help guide the development of targeted strategies to protect immune function during infection.
Overriding impaired FPR chemotaxis signaling in diabetic neutrophil stimulates infection control in murine diabetic wound. eLife, 2022.
This study demonstrates that impaired neutrophil migration contributes to poor infection control in diabetic wounds. Restoring neutrophil chemotaxis offers a potential therapeutic strategy to strengthen the body's ability to fight infection and promote wound repair.
IL-10 Dysregulation Underlies Chemokine Insufficiency, Delayed Macrophage Response, and Impaired Healing in Diabetic Wounds. Journal of Investigative Dermatology. 2022.
Identifies a mechanism linking IL-10 dysregulation, chemokine insufficiency, macrophage dysfunction, and impaired diabetic wound healing, directly supporting the lab's current immunology and wound-healing program.
Apoptosis and Compensatory Proliferation Signaling Are Coupled by CrkI-Containing Microvesicles. Dev Cell. 2017
This work moved beyond pathogen biology to reveal a fundamental mechanism connecting apoptosis with compensatory proliferation, identifying CrkI-containing microvesicles as signaling mediators.
Publications
1. Pseudomonas aeruginosa Type III-Secreted Toxin ExoT Inhibits Host-Cell Division by Targeting Cytokinesis at Multiple Steps
1. Pseudomonas aeruginosa Type III-Secreted Toxin ExoT Inhibits Host-Cell Division by Targeting Cytokinesis at Multiple Steps
Shafikhani SH, Engel J.
Proceedings of the National Academy of Sciences (PNAS). 2006;103(42):15605–15610.
DOI: 10.1073/pnas.0605949103
2. Pseudomonas aeruginosa ExoT Induces Atypical Anoikis Apoptosis in Target Host Cells by Transforming Crk Adaptor Protein into a Cytotoxin
2. Pseudomonas aeruginosa ExoT Induces Atypical Anoikis Apoptosis in Target Host Cells by Transforming Crk Adaptor Protein into a Cytotoxin
Wood S, Goldufsky J, Shafikhani SH.
PLOS Pathogens. 2015;11(5):e1004934.
DOI: 10.1371/journal.ppat.1004934
3. Apoptosis and Compensatory Proliferation Signaling Are Coupled by CrkI-Containing Microvesicles
3. Apoptosis and Compensatory Proliferation Signaling Are Coupled by CrkI-Containing Microvesicles
Gupta KH, Goldufsky JW, Wood SJ, et al., Shafikhani SH.
Developmental Cell. 2017;41(6):674–684.e5.
DOI: 10.1016/j.devcel.2017.05.014
4. CrkII/Abl Phosphorylation Cascade Is Critical for NLRC4 Inflammasome Activity and Is Blocked by Pseudomonas aeruginosa ExoT
Mohamed MF, Gupta K, Goldufsky JW, et al., Shafikhani SH.
Nature Communications. 2022;13:1295.
DOI: 10.1038/s41467-022-28967-5
5. Overriding Impaired FPR Chemotaxis Signaling in Diabetic Neutrophil Stimulates Infection Control in Murine Diabetic Wound
5. Overriding Impaired FPR Chemotaxis Signaling in Diabetic Neutrophil Stimulates Infection Control in Murine Diabetic Wound
Roy R, Zayas J, Singh SK, et al., Shafikhani SH.
eLife. 2022;11:e72071.
DOI: 10.7554/eLife.72071
6. IL-10 Dysregulation Underlies Chemokine Insufficiency, Delayed Macrophage Response, and Impaired Healing in Diabetic Wounds
6. IL-10 Dysregulation Underlies Chemokine Insufficiency, Delayed Macrophage Response, and Impaired Healing in Diabetic Wounds
Roy R, Zayas J, Mohamed MF, et al., Shafikhani SH.
Journal of Investigative Dermatology. 2022;142(3):692–704.e14.
DOI: 10.1016/j.jid.2021.08.428
7. Pseudomonas aeruginosa Uses T3SS to Inhibit Diabetic Wound Healing
7. Pseudomonas aeruginosa Uses T3SS to Inhibit Diabetic Wound Healing
Goldufsky J, Wood SJ, Jayaraman V, et al., Shafikhani SH.
Wound Repair and Regeneration. 2015;23(4):557–564.
DOI: 10.1111/wrr.12310
8. Pseudomonas aeruginosa ExoT Induces Mitochondrial Apoptosis in Target Host Cells in a Manner That Depends on Its GTPase-Activating Protein (GAP) Domain Activity
8. Pseudomonas aeruginosa ExoT Induces Mitochondrial Apoptosis in Target Host Cells in a Manner That Depends on Its GTPase-Activating Protein (GAP) Domain Activity
Wood SJ, Goldufsky J, Bello D, et al., Shafikhani SH.
Journal of Biological Chemistry. 2015;290(48):29063–29073.
DOI: 10.1074/jbc.M115.689950
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