Supplementary Materials for
Identification of ROCK1 as an Upstream Activator of the JIP-3 to JNK Signaling Axis in Response to UVB Damage
Pat P. Ongusaha,1 Hank H. Qi,2 Lakshmi Raj,1 Young-Bum Kim,3 Stuart A. Aaronson,4 Roger J. Davis,5 Yang Shi,2 James K. Liao,6 Sam W. Lee1*
1Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, 13th Street, Building 149, Charlestown, MA 02129, USA.
2Department of Pathology, Harvard Medical School, NRB 854, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
3Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
4Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
5Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
6Vascular Medicine Research Unit, Brigham and Women�s Hospital and Harvard Medical School, 65 Landsdowne Street, Room 275, Cambridge, MA 02139, USA.
This PDF file includes:
- Fig. S1. The kinase domain of ROCK1 is involved in binding to JIP-3.
- Fig. S2. Glycerol gradient analysis of ROCK1 and JIP-3.
- Fig. S3. Depletion of ROCK1 compromises UVB-induced apoptosis.
- Fig. S4. Ectopic expression of ROCK1 in ROCK1-depleted HACAT cells rescued the ROCK1-suppression phenotype.
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