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. 2012 Jun 15;6:70. doi: 10.1186/1752-0509-6-70

Figure 1.

Figure 1

Schematics relevant to this study.a, A portion of the regulatory domain of IP3R1 and the C-terminal, adapted from [21,22], with the PP1 binding motif and mutations for ITPR118/18 and ITPR1op1/opt mice. b, Summary of various aspects of this study. IP3R1 is the center of this study, involved in phosphoinositol signaling, calcium release, membrane potential modulation; the dysregulation of any of these functions may lead to ataxia.