ANNA HUTTENLOCHER, MD

Research

Our research focuses on characterizing the molecular mechanisms that regulate cell migration. Implications to tumor metastasis and inflammation are also areas of interest. We are interested in how environmental stimuli affect cell migration and inflammation using both in vitro and in vivo approaches. A core focus of our current work is the development of novel transgenic zebrafish models that are being used to study cell motility and inflammation in vivo. The generation of transgenic zebrafish that have GFP-labeled neutrophils, and the identification of chronic inflammation mutants from genetic screens, have provided unique and powerful systems to study inflammation in real time.

Cell surface adhesion receptors, including integrins and cadherins, play a central role in during cell migration. Our previous studies have demonstrated that cell migration speed and cell invasiveness are modulated by integrin-ligand binding affinity and cytoskeletal linkages. We have recently identified the calcium-dependent protease calpain as a regulator of integrin-cytoskeletal interactions during cell migration. Specifically we find that calpain modulates integrin-cytoskeletal interactions and cell detachment.

Publications

• Mathias JR, Dodd ME, Walters KB, Rhodes J, Kanki JP, Look AT, Huttenlocher A. Live imaging of chronic inflammation caused by mutation of zebrafish Hai1. J Cell Sci. 2007; 120:3372-83.
• Chan KT, Cortesio CL, Huttenlocher A. Integrins in cell migration. Methods Enzymol. 2007;426:47-67.
• Doan AT, Huttenlocher A. RACK1 regulates Src activity and modulates paxillin dynamics during cell migration. Exp Cell Res. 2007; 313:2667-79.
• Nuzzi PA, Lokuta MA, Huttenlocher A. Analysis of neutrophil chemotaxis. Methods Mol Biol. 2007;370:23-36.
• Huttenlocher A, Horwitz AR. Wound healing with electric potential. N Engl J Med. 2007 356:303-4.

Mentor to METC Post-Docs:

• Davalyn Powell (2014-2016)
• Emily Rosowski (2013-2014)
• Christina Freisinger (2010-2011)
• Peter Cavnar (2008-2010)