Polycomb Group Proteins as Epigenetic Mediators of Neuroprotection in Ischemic Tolerance

Martha Stapels, Chelsea Piper, Tao Yang, Minghua Li, Cheri Stowell, Zhi-gang Xiong, Julie Saugstad, Roger P. Simon,* Scott Geromanos, James Langridge, Jing-quan Lan, An Zhou*

*To whom correspondence should be addressed. E-mail: azhou{at}downeurobiology.org (A.Z.) and rsimon{at}downeurobiology.org (R.P.S.)

This PDF file includes:

• Fig. S1. Chromatographic peak area measurement.
• Fig. S2. Immunohistochemistry of H2A and BMI1.
• Fig. S3. Knocking down or overexpressing PcG proteins.
• Fig. S4. Changes in abundance of RING2 and mUb-H2A in mouse brains and in NS20Y cells.
• Table S1. Total identified and quantified proteins in mouse cortex.
• Table S2. Numbers of proteins that change in abundance under each condition.
• Table S3. Proteins that change in abundance under ischemic-preconditioned condition.
• Table S4. Proteins that change in abundance under ischemic-tolerant condition.
• Table S5. Proteins that change in abundance under ischemic-injured condition.
• Table S6. Proteins that change in abundance under a unique brain ischemic condition or more than one condition.
• Table S7. Biological processes presented by proteins that change in abundance under different conditions of brain ischemia.

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