Abl Family Kinases Modulate T Cell–Mediated Inflammation and Chemokine-Induced Migration Through the Adaptor HEF1 and the GTPase Rap1

Jing Jin Gu, Catherine P. Lavau, Elena Pugacheva, Erik J. Soderblom, M. Arthur Moseley, Ann Marie Pendergast*

*To whom correspondence should be addressed. E-mail: ann.pendergast{at}duke.edu

This PDF file includes:

• Materials and Methods
• Fig. S1. Chemokine-induced activation of Abl family kinases and signaling in T cells.
• Fig. S2. Defective SDF-1α–induced migration in T cell blasts depleted of Abl family kinases.
• Fig. S3. Cell surface amounts of chemokine receptors and β₁ integrin are unaffected by loss of functional Abl family kinases.
• Fig. S4. Expression of active Rap1 rescues the defective migration of Abl/Arg null T cells.
• Fig. S5. Integrin-mediated binding to VCAM and ICAM in the absence of functional Abl family kinases.
• Fig. S6. Abl family kinases associate with and phosphorylate HEF1.
• Fig. S7. Identification of HEF1 tyrosine residues that are phosphorylated by Abl family kinases.
• Fig. S8. Abl family kinases modulate inflammatory responses in CHS.
• Fig. S9. Analysis of cell surface markers on WT and Abl/Arg null T cells after hapten sensitization.
• Legends for Movies S1 to S4
• References

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Technical Details

Format: Adobe Acrobat PDF

Size: 1 MB

Other Supplementary Material for this manuscript includes the following:

• Movie S1 (.mov format). Motility of primary T cells in the absence of chemokines.
• Movie S2 (.mov format). Chemokinesis is impaired in T cells lacking Abl and Arg.
• Movies S3 and S4 (.mov format). The WT cells (green, movie S3) and Abl/Arg null cells (red, movie S4) that were used in movie S2 were tracked and cell movement was overlaid as indicated.

© 2012 American Association for the Advancement of Science