Supplementary Materials

Supplementary Materials for:

HES1 Is a Master Regulator of Glucocorticoid Receptor–Dependent Gene Expression

Javier R. Revollo, Robert H. Oakley, Nick Z. Lu, Mahita Kadmiel, Maheer Gandhavadi, John A. Cidlowski*

*Corresponding author. E-mail: cidlows1@niehs.nih.gov

This PDF file includes:

  • Fig. S1. The GR Dim4 DNA binding mutant represses HES1 expression.
  • Fig. S2. Conservation of the HES1 NFκB site across species.
  • Fig. S3. Overexpression of HES1 silences various genes.
  • Fig. S4. Absence of HES1 increases glucocorticoid sensitivity.
  • Fig. S5. Absence of HES1 elicits a faster response to glucocorticoid signaling.
  • Fig. S6. Notch signaling inhibits glucocorticoid actions through HES1.
  • Fig. S7. HES1 and GR do not physically interact.
  • Fig. S8. Expression of Flag-WT-HES1 and Flag-mut-HES1.
  • Fig. S9. Glucocorticoids repress HES1 gene expression in multiple tissues.
  • Fig. S10. Absence of HES1 potentiates GR-mediated induction of G6P and PEPCK.
  • Fig. S11. Insulin concentrations.

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Citation: J. R. Revollo, R. H. Oakley, N. Z. Lu, M. Kadmiel, M. Gandhavadi, J. A. Cidlowski, HES1 is Amaster Regulator of Glucocorticoid Receptor–Dependent Gene Expression. Sci. Signal. 6, ra103 (2013).

© 2013 American Association for the Advancement of Science