2016
DOI: 10.18632/aging.101051
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Abstract: Mitochondrial proteases ensure mitochondrial integrity and function after oxidative stress by providing mitochondrial protein quality control. However, the molecular mechanisms that regulate this basic biological function in eukaryotic cells remain largely unknown. Caveolin-1 is a scaffolding protein involved in signal transduction. We find that AFG3L2, a m-AAA type of mitochondrial protease, is a novel caveolin-1-interacting protein in vitro. We show that oxidative stress promotes the translocation of both ca… Show more

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Cited by 21 publications
(11 citation statements)
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References 57 publications
(67 reference statements)
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“…p63 is a member of the p53 family of transcription factors and the absence of expression of one of its isoforms, TAp63, has been shown to lead to senescence and premature aging of epidermal and dermal precursors 28 . Caveolin is thought to have a tumor-suppressor function at early stages of malignant transformation 29 , to contribute to immune senescence 30 and the ability of aged cells to respond to oxidative stress 31 . Our finding of reduced miR-203-3p expression in long-lived mouse strains may be indicative of a phenotype in which cells have greater proliferative and adaptive capacity alongside a reduced propensity to become senescent, all of which could create favorable conditions for increased longevity.…”
Section: Discussionmentioning
confidence: 99%
“…p63 is a member of the p53 family of transcription factors and the absence of expression of one of its isoforms, TAp63, has been shown to lead to senescence and premature aging of epidermal and dermal precursors 28 . Caveolin is thought to have a tumor-suppressor function at early stages of malignant transformation 29 , to contribute to immune senescence 30 and the ability of aged cells to respond to oxidative stress 31 . Our finding of reduced miR-203-3p expression in long-lived mouse strains may be indicative of a phenotype in which cells have greater proliferative and adaptive capacity alongside a reduced propensity to become senescent, all of which could create favorable conditions for increased longevity.…”
Section: Discussionmentioning
confidence: 99%
“…Another study also demonstrated that Cav-1 deficiency could increase the mitochondrial membrane condensation, accompanied with dysfunction of respiratory chain efficiency and intrinsic antioxidant defense [ 196 ]. Mechanism study further validated that Cav-1 loss resulted in the cytoplasmic and proteasome-dependent degradation of complexes I, III, IV, and V but had no effects on either mitochondrial number or morphology [ 197 ]. All these findings suggested that strategies targeting Cav-1 translocation to mitochondrion might be a novel approach for cancer prevention.…”
Section: Therapeutic Implication Of Cav-1-targeted Treatment For Cmentioning
confidence: 99%
“…In E11 podocytes, cav-1 OE attenuated H 2 O 2 -induced oxidative stress responses and preserved mitochondrial function, as well as significantly suppressing apoptosis [153]. Moreover, various cav-1-deficient cells have displayed mitochondrial dysfunction including impaired energy generation, and increased mitochondrial ROS production [154156]. Based on the abovementioned findings, we speculate that cav-1 could relay apoptotic signaling via allowing Fas multimerization, but also attenuates apoptosis through preventing mitochondrial dysfunction.…”
Section: Important Role Of Cav-1 In Ismentioning
confidence: 99%