Cell Migration: Tunable Substrates Unveil Chemical Complementation of a Genetic Cell Migration Defect (Adv. Healthcare Mater. 8/2013)

Authors

  • Janina Kristin Hellmann,

    1. Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany
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  • Nadine Perschmann,

    1. Department of New Materials and Biosystems, Max Planck Institute for Intelligent Systems and Department of Biophysical Chemistry, University of Heidelberg, Postal address: Heisenbergstr. 3, 70569 Stuttgart, Germany
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  • Joachim P. Spatz,

    Corresponding author
    1. Department of New Materials and Biosystems, Max Planck Institute for Intelligent Systems and Department of Biophysical Chemistry, University of Heidelberg, Postal address: Heisenbergstr. 3, 70569 Stuttgart, Germany
    • Joachim P. Spatz, Department of New Materials and Biosystems, Max Planck Institute for Intelligent Systems and Department of Biophysical Chemistry, University of Heidelberg, Postal address: Heisenbergstr. 3, 70569 Stuttgart, Germany.

      Friedrich Frischknecht, Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany

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  • Friedrich Frischknecht

    Corresponding author
    1. Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany
    • Joachim P. Spatz, Department of New Materials and Biosystems, Max Planck Institute for Intelligent Systems and Department of Biophysical Chemistry, University of Heidelberg, Postal address: Heisenbergstr. 3, 70569 Stuttgart, Germany.

      Friedrich Frischknecht, Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany

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Abstract

original image

Sporozoite motility is essential for malaria transmission and constitutes the first target for intervention within the human body. On page 1162 J. P. Spatz, F. Frischknecht, and co-workers use a set of tunable substrates with changed ligand spacing and elasticity to show that a small chemical compound that stabilizes the actin cytoskeleton can compensate the motility defects of parasites that lack a surface protein important for substrate adhesion.

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