Supplementary Materials

Supplementary Materials for:

DDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress

Bridget Simonson, Vinita Subramanya, Mun Chun Chan, Aifeng Zhang, Hannabeth Franchino, Filomena Ottaviano, Manoj K. Mishra, Ashley C. Knight, Danielle Hunt, Ionita Ghiran, Tejvir S. Khurana, Maria I. Kontaridis, Anthony Rosenzweig, Saumya Das*

*Corresponding author. Email: sdas{at}partners.org

This PDF file includes:

  • Fig. S1. DDiT4 is differentially regulated compared to DDiT4L.
  • Fig. S2. Regulation of mTOR signaling by DDiT4L under different conditions in NRVMs.
  • Fig. S3. Conditional heart-specific overexpression of DDiT4L.
  • Fig. S4. Acute increases in DDiT4L lead to alterations in mTORC1 signaling but not in systolic function.
  • Fig. S5. Overexpression of DDiT4L does not alter the phosphorylation of IRS1.
  • Table S1. Top 20 candidates from DSAGE screen of genes with increased expression in SGK-CA mice compared to other transgenic mice.
  • Table S2. DDiT4L/tTA mice have mild diastolic dysfunction, which is reversed upon transgene suppression.
  • Table S3. Mouse primers.
  • Table S4. Rat primers.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Raw DSAGE data file.

Citation: B. Simonson, V. Subramanya, M. C. Chan, A. Zhang, H. Franchino, F. Ottaviano, M. K. Mishra, A. C. Knight, D. Hunt, I. Ghiran, T. S. Khurana, M. I. Kontaridis, A. Rosenzweig, S. Das, DDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress. Sci. Signal. 10, eaaf5967 (2017).

© 2017 American Association for the Advancement of Science