Supplementary Materials

Supplementary Materials for:

Coincident signals from GPCRs and receptor tyrosine kinases are uniquely transduced by PI3Kβ in myeloid cells

Daniel M. Houslay, Karen E. Anderson, Tamara Chessa, Suhasini Kulkarni, Ralph Fritsch, Julian Downward, Jonathan M. Backer, Len R. Stephens,* Phillip T. Hawkins*

*Corresponding author. Email: phillip.hawkins{at}babraham.ac.uk (P.T.H.); len.stephens{at}babraham.ac.uk (L.R.S.)

This PDF file includes:

  • Methods
  • Fig. S1. Targeting of Pik3cbKK526,527DD.
  • Fig. S2. Confirmation of the correct targeting of Pik3cbKK526,527DD.
  • Fig. S3. p110β quantities in BMDMs and BMNs are unaffected by the introduction of the RBD- and Gβγ-insensitive mutations.
  • Fig. S4. Dose responses of GPCR (C5a) and RTK (M-CSF) agonists on PIP3 production by BMDMs.
  • Fig. S5. ROS generation in BMNs in response to the phagocytosis of IgG-SRBCs, but not soluble GPCR agonists, requires p110β activity.
  • Fig. S6. ROS generation in BMNs in response to adhesion to poly-RGD+, but not immune complexes, is independent of BLT1 activation.
  • Reference (70)

[Download PDF]

Technical Details

Format: Adobe Acrobat PDF

Size: 590 KB


Citation: D. M. Houslay, K. E. Anderson, T. Chessa, S. Kulkarni, R. Fritsch, J. Downward, J. M. Backer, L. R. Stephens, P. T. Hawkins, Coincident signals from GPCRs and receptor tyrosine kinases are uniquely transduced by PI3Kβ in myeloid cells. Sci. Signal. 9, ra82 (2016).

© 2016 American Association for the Advancement of Science