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Sci. Signal., 19 June 2012
[DOI: 10.1126/scisignal.2003111]

Supplementary Materials for:

Direct Modification and Activation of a Nuclear Receptor–PIP2 Complex by the Inositol Lipid Kinase IPMK

Raymond D. Blind, Miyuki Suzawa, Holly A. Ingraham*

*To whom correspondence should be addressed. E-mail: holly.ingraham{at}ucsf.edu

This PDF file includes:

  • Fig. S1. p110γ, the kinase-dead rIPMK mutant (D127A), and IP3K fail to generate PIP3 from SF-1–PIP2.
  • Fig. S2. Enzyme/substrate kinetic parameters and competitive inhibition by Ins(1,4,5)P of IPMK activity on SF-1–PIP2.
  • Fig. S3. Overexpression of different IPMKs does not affect SF-1 transcript abundance.
  • Fig. S4. SF-1 transcript abundance and SF-1 nuclear localization are unaffected by ATA and EGCG, and wortmannin does not recapitulate ATA effects on SF-1 target gene expression.
  • Fig. S5. SF-1 purified from HEK 293 cells is not phosphorylated by IPMK.
  • Table S1. RT-qPCR primers.
  • Table S2. ChIP-qPCR primers.

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Citation: R. D. Blind, M. Suzawa, H. A. Ingraham, Direct Modification and Activation of a Nuclear Receptor–PIP2 Complex by the Inositol Lipid Kinase IPMK. Sci. Signal. 5, ra44 (2012).

© 2012 American Association for the Advancement of Science


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