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  1. Article: Beyond being an energy supplier, ATP synthase is a sculptor of mitochondrial cristae

    Miranda-Astudillo, Héctor / Ostolga-Chavarría, Marcos / Cardol, Pierre / González-Halphen, Diego

    Biochimica et biophysica acta. 2022 Aug. 01, v. 1863, no. 6

    2022  

    Abstract: Mitochondrial F₁FO-ATP synthase plays a key role in cellular bioenergetics; this enzyme is present in all eukaryotic linages except in amitochondriate organisms. Despite its ancestral origin, traceable to the alpha proteobacterial endosymbiotic event, ... ...

    Abstract Mitochondrial F₁FO-ATP synthase plays a key role in cellular bioenergetics; this enzyme is present in all eukaryotic linages except in amitochondriate organisms. Despite its ancestral origin, traceable to the alpha proteobacterial endosymbiotic event, the actual structural diversity of these complexes, due to large differences in their polypeptide composition, reflects an important evolutionary divergence between eukaryotic lineages. We discuss the effect of these structural differences on the oligomerization of the complex and the shape of mitochondrial cristae.
    Keywords H-transporting ATP synthase ; divergent evolution ; energy ; energy metabolism ; mitochondria ; oligomerization ; polypeptides
    Language English
    Dates of publication 2022-0801
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 282711-6
    ISSN 0005-2728 ; 0304-4173
    ISSN 0005-2728 ; 0304-4173
    DOI 10.1016/j.bbabio.2022.148569
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  2. Article ; Online: Beyond being an energy supplier, ATP synthase is a sculptor of mitochondrial cristae.

    Miranda-Astudillo, Héctor / Ostolga-Chavarría, Marcos / Cardol, Pierre / González-Halphen, Diego

    Biochimica et biophysica acta. Bioenergetics

    2022  Volume 1863, Issue 6, Page(s) 148569

    Abstract: Mitochondrial ... ...

    Abstract Mitochondrial F
    MeSH term(s) Adenosine Triphosphate/metabolism ; Glycogen Synthase/metabolism ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism ; Mitochondrial Proton-Translocating ATPases/metabolism
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; Glycogen Synthase (EC 2.4.1.11) ; Mitochondrial Proton-Translocating ATPases (EC 3.6.3.-)
    Language English
    Publishing date 2022-05-14
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbabio.2022.148569
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  3. Article ; Online: Actin-Cytoskeleton Drives Caveolae Signaling to Mitochondria during Postconditioning.

    Correa, Francisco / Enríquez-Cortina, Cristina / Silva-Palacios, Alejandro / Román-Anguiano, Nadia / Gil-Hernández, Aurora / Ostolga-Chavarría, Marcos / Soria-Castro, Elizabeth / Hernández-Rizo, Sharik / de Los Heros, Paola / Chávez-Canales, María / Zazueta, Cecilia

    Cells

    2023  Volume 12, Issue 3

    Abstract: Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning. In this work, we evaluated the role that the actin-cytoskeleton network ... ...

    Abstract Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning. In this work, we evaluated the role that the actin-cytoskeleton network exerts on caveolae-mitochondria communication during postconditioning. Isolated rat hearts subjected to I/R and to postconditioning were treated with latrunculin A, a cytoskeleton disruptor. Cardiac function was compared between these hearts and those exposed only to I/R and to the cardioprotective maneuver. Caveolae and mitochondria structures were determined by electron microscopy and maintenance of the actin-cytoskeleton was evaluated by phalloidin staining. Caveolin-3 and other putative caveolae-conforming proteins were detected by immunoblot analysis. Co-expression of caveolin-3 and actin was evaluated both in lipid raft fractions and in heart tissue from the different groups. Mitochondrial function was assessed by respirometry and correlated with cholesterol levels. Treatment with latrunculin A abolishes the cardioprotective postconditioning effect, inducing morphological and structural changes in cardiac tissue, reducing F-actin staining and diminishing caveolae formation. Latrunculin A administration to post-conditioned hearts decreases the interaction between caveolae-forming proteins, the co-localization of caveolin with actin and inhibits oxygen consumption rates in both subsarcolemmal and interfibrillar mitochondria. We conclude that actin-cytoskeleton drives caveolae signaling to mitochondria during postconditioning, supporting their functional integrity and contributing to cardiac adaption against reperfusion injury.
    MeSH term(s) Rats ; Animals ; Caveolae/metabolism ; Actins/metabolism ; Caveolin 3/metabolism ; Cytoskeleton/metabolism ; Caveolin 1/metabolism ; Reperfusion Injury/metabolism ; Mitochondria/metabolism
    Chemical Substances latrunculin A (SRQ9WWM084) ; Actins ; Caveolin 3 ; Caveolin 1
    Language English
    Publishing date 2023-02-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12030492
    Database MEDical Literature Analysis and Retrieval System OnLINE

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