Julie L. Kadrmas, Ph.D.

Research Interests

  • Metastasis
  • Integrin Signaling
  • Integrin Adhesion
  • Cell Migration
  • Drosophila melanogaster

Languages

  • English

Academic Information

  • Departments: Oncological Sciences - Research Assistant Professor
  • Cancer Center Programs: Cell Response & Regulation

Academic Office Information

  • (801) 587-4634
  • Huntsman Cancer Institute
    Department of Oncological Sciences
    2000 Circle of Hope, Room: 5343
    Salt Lake City, UT 84112

Academic Bio

Julie Kadrmas, Ph.D. is an investigator in the Cell Response and Regulation Program at the Huntsman Cancer Institute. Her group is interested in understanding regulatory mechanisms controlling cell adhesion and migration, with implications for how cancer cells gain the capacity to leave the site of a primary tumor and migrate during metastasis. Through the examination of normal developmental processes in the fruit fly Drosophila melanogaster, they characterize the functions of the integrin family of transmembrane receptors in regulating cell attachment and movement. Of particular interest is a molecular scaffolding protein called PINCH, which physically associates with integrins, as well as several additional PINCH protein partners that impinge upon distinct signaling cascades. Their work will provide a molecular understanding of how protein-protein interactions mediated by molecular scaffolds such as PINCH, integrate signals between multiple pathways to coordinate complex biological processes like cell adhesion and migration.

Education History

Type School Degree
Postdoctoral Fellowship University of Utah, Department of Chemistry
Chemistry
Postdoctoral Fellow
Doctoral Training Duke University
Biochemistry
Ph.D.
Fellowship Duke University, National Institutes of Health
Pharmacology
Fellow
Undergraduate Bowling Green State University
Biology & Chemistry
B.S.

Selected Publications

Journal Article

  1. Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants.Pronovost SM, Beckerle MC, Kadrmas JL (2013). Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants. PLoS Genet, 9(3), e1003406.
  2. Drosophila melanogaster muscle LIM protein and alpha-actinin function together to stabilize muscle cytoarchitecture: a potential role for Mlp84B in actin-crosslinking.Clark KA, Kadrmas JL (2013). Drosophila melanogaster muscle LIM protein and alpha-actinin function together to stabilize muscle cytoarchitecture: a potential role for Mlp84B in actin-crosslinking. Cytoskeleton (Hoboken), 70(6), 304-16.
  3. Interactions by 2D Gel Electrophoresis Overlap (iGEO): a novel high fidelity approach to identify constituents of protein complexes.Yoshigi M, Pronovost SM, Kadrmas JL (2013). Interactions by 2D Gel Electrophoresis Overlap (iGEO): a novel high fidelity approach to identify constituents of protein complexes. Proteome Sci, 11(1), 21.
  4. Elias MC, Pronovost SM, Cahill KJ, Beckerle MC and Kadrmas JL (2012). A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted. J Cell Sci, 125, 3185-3194.
  5. Characterization of RACK1 function in Drosophila development.Kadrmas JL, Smith MA, Pronovost SM, Beckerle MC (2007). Characterization of RACK1 function in Drosophila development. Dev Dyn, 236(8), 2207-15.
  6. The integrin effector PINCH regulates JNK activity and epithelial migration in concert with Ras suppressor 1.Kadrmas JL, Smith MA, Clark KA, Pronovost SM, Muster N, Yates JR 3rd, Beckerle MC (2004). The integrin effector PINCH regulates JNK activity and epithelial migration in concert with Ras suppressor 1. J Cell Biol, 167(6), 1019-24.

Review

  1. The LIM domain: from the cytoskeleton to the nucleus.Kadrmas JL, Beckerle MC (2004). The LIM domain: from the cytoskeleton to the nucleus. [Review]. Nat Rev Mol Cell Biol, 5(11), 920-31.