Apolipoproteins L1 and L3 Control Mitochondrial Membrane Dynamics
Dynamics
DOI:
10.2139/ssrn.4510521
Publication Date:
2023-07-18T18:21:50Z
AUTHORS (9)
ABSTRACT
Apolipoproteins-L1 and -L3 (APOLs) are associated at the Golgi membrane with phosphatidylinositol-4-kinase-IIIB (PI4KB) non-muscular-myosin-2A (NM2A). Either APOL1 C-terminal truncation (APOL1Δ) or APOL3 deletion (APOL3-KO) reduces PI4KB activity triggers actomyosin reorganization. We report that APOL3, but not APOL1, controls through interaction neuronal-calcium-sensor-1 (NCS1) calneuron-1 (CALN1). Both APOLs present in Golgi-derived autophagy-related-protein-9A (ATG9A) vesicles, involved trafficking. Like APOL3-KO, APOL1Δ induces dissociation from decreasing mitophagy flux reduction of mitochondrial fission fusion, triggering production reactive oxygen species. respectively, bind to receptor prohibitin-2 (PHB2) mitophagosome fusion protein vesicle-associated-membrane-protein-8 (VAMP8). While APOL1-PHB2 may condition targeting PI4KB, APOL3-VAMP8 promotes enhanced by cardiolipin. propose dynamics interactions factor VAMP8.
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