Reply to: The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria
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Publisher
Springer Science and Business Media LLC
Link
https://www.nature.com/articles/s41467-024-51448-w.pdf
Reference12 articles.
1. Li, L. Y., Luo, X. & Wang, X. Endonuclease G is an apoptotic DNase when released from mitochondria. Nature 412, 95–99 (2001).
2. Arnoult, D. et al. Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization. EMBO J. 22, 4385–4399 (2003).
3. David, K. K., Sasaki, M., Yu, S. W., Dawson, T. M. & Dawson, V. L. EndoG is dispensable in embryogenesis and apoptosis. Cell Death Differ. 13, 1147–1155 (2006).
4. Yang, S. et al. AKT2 blocks nucleus translocation of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) while promoting caspase activation during cardiac ischemia. Int. J. Mol. Sci. 18, 565 (2017).
5. Li, S. et al. Picroside II exerts a neuroprotective effect by inhibiting mPTP permeability and EndoG release after cerebral ischemia/reperfusion injury in rats. J. Mol. Neurosci. 64, 144–155 (2018).
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