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the results of this study identified MARCH5 as a candidate oncogene in ovarian cancer and a potential target for ovarian cancer therapy.
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MARCH5 directly interacts with FUNDC1 to mediate its ubiquitylation at lysine 119 for subsequent degradation.
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These findings and data showing MARCH5-dependent degradation of MiD49 upon stress support the possibility that MARCH5 regulation of MiD49 is a novel mechanism controlling mitochondrial fission and, consequently, the cellular response to stress.
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Self-clearance mechanism of mitochondrial ligase MARCH5 contributes to mitochondria quality control.MARCH5 is regulated by auto-ubiquitination.
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MARCH5 binds MAVS only during viral stimulation when MAVS forms aggregates, and these interactions require the RING domain of MARCH5 and the CARD domain of MAVS.
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Our results indicate that HDAC6 is a critical regulator of MFN2 degradation by MARCH5, thus protecting mitochondrial connectivity from hypoxic stress.
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A fine balance of Mfn1 levels is maintained by MARCH5-mediated quality control on acetylated Mfn1.
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MITOL regulates ER tethering to mitochondria by activating Mfn2 via K192 ubiquitination.
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balance between LC1 activation by S-nitrosylation and down-regulation by MITOL is critical for neuronal cell survival
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MARCH5 is an authentic E3 ubiquitin ligase and catalyzes K63-linked polyubiquitination of TANK. MARCH5 modulates TLR7 signaling via releasing the inhibitory action of TANK toward TRAF6.
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study found that MITOL interacts with and ubiquitinates DeltaNAT-3Q71, a pathogenic ataxin-3 mutant, in mitochondria and attenuates its toxicity
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lack of MARCH5 results in mitochondrial elongation, which promotes cellular senescence by blocking Drp1 activity and/or promoting accumulation of Mfn1 at the mitochondria
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Results indicate that MITOL plays a protective role against mitochondrial dysfunction caused by the mitochondrial accumulation of mSOD1 via the ubiquitin-proteasome pathway.
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A novel mitochondrial ubiquitin ligase, designated MITOL, which is localized in the mitochondrial outer membrane, plays a critical role in mitochondrial dynamics through the control of mitochondrial fission proteins.
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MARCH-V has a crucial role in the control of mitochondrial morphology by regulating MFN2 and Drp1 activities.
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MARCH5 is required for DRP1-dependent mitochondrial division.
