Supplementary Materials

Supplementary Materials for:

A FAK-Cas-Rac-Lamellipodin Signaling Module Transduces Extracellular Matrix Stiffness into Mechanosensitive Cell Cycling

Yong Ho Bae,* Keeley L. Mui, Bernadette Y. Hsu, Shu-Lin Liu, Alexandra Cretu, Ziba Razinia, Tina Xu, Ellen Puré, Richard K. Assoian*

*Corresponding author. E-mail: yob@mail.med.upenn.edu (Y.H.B.); assoian@mail.med.upenn.edu (R.K.A.)

This PDF file includes:

  • Fig. S1. Stiffness-dependent regulation of focal adhesion proteins and cell cycling.
  • Fig. S2. Effect of time and stiffness-dependent Rac activity on intracellular stiffness.
  • Fig. S3. Regulation of Rac activity by CrkII.
  • Fig. S4. A FAK-Cas signaling module is necessary for cyclin D1 induction in MEFs and VSMCs.
  • Fig. S5. Bioinformatic identification of a FAK/Rac signaling pathway to cyclin D1.
  • Fig. S6. Morphology of uninjured femoral arteries from Rac1fl/fl;SM-iCre mice.
  • Fig. S7. Effect of lamellipodin knockdown on FAK and Cas phosphorylation and cyclin D1 induction.
  • Fig. S8. Dose-dependent inhibition of FAK autophosphorylation and Rac-GTP loading by PF573228 and NSC23766.
  • Table S1. Cell cycle genes that are differentially expressed after vascular injury.

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Citation: Y. H. Bae, K. L. Mui, B. Y. Hsu, S.-L. Liu, A. Cretu, Z. Razinia, T. Xu, E. Puré, R. K. Assoian, A FAK-Cas-Rac-Lamellipodin Signaling Module Transduces Extracellular Matrix Stiffness into Mechanosensitive Cell Cycling. Sci. Signal. 7, ra57 (2014).

© 2014 American Association for the Advancement of Science