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Git1-PGK1 interaction results in self-protection against spinal cord ischemia-reperfusion injury by modulating KEAP1–Nrf2 signaling. Binding of Git1 to PGK1 restricts PGK1 phosphorylation leading to increased glucose metabolism intermediates, ultimately promoting dimerization of Keap1 and reducing ubiquitination of Nrf2, leading to better antioxidant capacity of neurons and better functional recovery after SCIRI.
