Extended Data Fig. 4: MCM8 mediates a mitophagy pathway that is independent of PINK1, PRKN, NIX, FUNDC1 and DRP1. | Nature Cardiovascular Research

Extended Data Fig. 4: MCM8 mediates a mitophagy pathway that is independent of PINK1, PRKN, NIX, FUNDC1 and DRP1.

From: MCM8-mediated mitophagy protects vascular health in response to nitric oxide signaling in a mouse model of Kawasaki disease

Extended Data Fig. 4: MCM8 mediates a mitophagy pathway that is independent of PINK1, PRKN, NIX, FUNDC1 and DRP1.

a, b, Immunoblot showing LC3B on isolated mitochondria (mitoLC3), as well as MCM8 and other mitochondrial proteins including TOM20, PINK1 and COXIV from the whole cell lysate (WCL) of empty vector (EV) or Flag-MCM8 transfected HeLa cells (a) or ctrl- or MCM8-siRNA transfected THP-1 cells (b). c, Flow cytometry showing mitophagic flux in ctrl- or MCM8- siRNA transfected mt-mKeima-HeLa cells. d, e, Dot plots showing the expression of IFNA (left) and immunoblot showing pIRF3 (right) in ctrl- or MCM8-siRNA transfected PINK1-deficient (d) or PRKN-deficient (e) THP-1 cells (n = 3 independent samples). f, g, h, Immunoblot showing IRF3 phosphorylation in ctrl- or MCM8-siRNA transfected NIX-deficient (f), FUNDC1-deficient (g) or DNM1L (DRP1)-deficient (h) THP-1 cells. i, Flow cytometry showing mitophagic flux in EV or MCM8 transfected PINK1-deficient, NIX-deficient, FUNDC1-deficient or DNM1L-deficient mt-mKeima-HeLa cells under indicated conditions. Data are mean ± s.d. P values were calculated by two-tailed Student’s t test for all experiments.

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