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:
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.
Format: Adobe Acrobat PDF
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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).