Supplementary Materials

Supplementary Materials for:

Maternal Hyperglycemia Activates an ASK1–FoxO3a–Caspase 8 Pathway That Leads to Embryonic Neural Tube Defects

Peixin Yang,* Xuezheng Li, Cheng Xu, Richard L. Eckert, E. Albert Reece, Horst Ronald Zielke, Fang Wang

*Corresponding author. E-mail: pyang@fpi.umaryland.edu

This PDF file includes:

  • Fig. S1. Anti–phospho-ASK1-Thr845 detects endogenous ASK1 phosphorylated at Thr845 and recombinant active ASK1.
  • Fig. S2. Maternal diabetes increases TRADD protein abundance and mRNA expression.
  • Fig. S3. Maternal diabetes does not affect nestin mRNA or protein abundance.
  • Fig. S4. Conditional deletion of the Casp8 gene in the neural tube does not recapitulate the lethal phenotype of germline Casp8 knockout mice.
  • Fig. S5. Breeding scheme to generate four genotypes of embryos from one mother under nondiabetic and diabetic conditions.
  • Fig. S6. Maternal Trx treatment reaches the embryo and restores the interaction between Trx and ASK1.
  • Fig. S7. Phosphorylation of FoxO3a was decreased in human neural tissues with NTDs.
  • Fig. S8. Summary diagram of the ASK1–FoxO3a–TRADD–caspase 8 cascade occurring hyperglycemia-induced apoptosis that leads to NTDs.
  • Table S1. Pregnancy outcomes at E10.5 in nondiabetic wild-type and Ask1−/− mice and diabetic wild-type and Ask1−/− mice.
  • Table S2. NTD rates in embryos of nondiabetic and diabetic wild-type mice, and diabetic FoxO3a−/− mice.
  • Table S3. Pregnancy outcomes at E10.5 in mice with or without hTrx treatment.
  • Table S4. Developmental outcome of cultured E8 embryos with or without hTrx treatment.
  • Table S5. Characteristics of human anencephaly and control cases.

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Citation: P. Yang, X. Li, C. Xu, R. L. Eckert, E. A. Reece, H. R. Zielke, F. Wang, Maternal Hyperglycemia Activates an ASK1–FoxO3a–Caspase 8 Pathway That Leads to Embryonic Neural Tube Defects. Sci. Signal. 6, ra74 (2013).

© 2013 American Association for the Advancement of Science