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Journal Abstract Search

478 related items for PubMed ID: 26415690

  • 1. Cardiolipin metabolism and its causal role in the etiology of the inherited cardiomyopathy Barth syndrome.
    Gaspard GJ, McMaster CR.
    Chem Phys Lipids; 2015 Dec; 193():1-10. PubMed ID: 26415690
    [Abstract] [Full Text] [Related]

  • 2. Barth syndrome: cellular compensation of mitochondrial dysfunction and apoptosis inhibition due to changes in cardiolipin remodeling linked to tafazzin (TAZ) gene mutation.
    Gonzalvez F, D'Aurelio M, Boutant M, Moustapha A, Puech JP, Landes T, Arnauné-Pelloquin L, Vial G, Taleux N, Slomianny C, Wanders RJ, Houtkooper RH, Bellenguer P, Møller IM, Gottlieb E, Vaz FM, Manfredi G, Petit PX.
    Biochim Biophys Acta; 2013 Aug; 1832(8):1194-206. PubMed ID: 23523468
    [Abstract] [Full Text] [Related]

  • 3. Cardiolipin remodeling: a regulatory hub for modulating cardiolipin metabolism and function.
    Ye C, Shen Z, Greenberg ML.
    J Bioenerg Biomembr; 2016 Apr; 48(2):113-23. PubMed ID: 25432572
    [Abstract] [Full Text] [Related]

  • 4. Mitochondrial dysfunctions in barth syndrome.
    Ghosh S, Iadarola DM, Ball WB, Gohil VM.
    IUBMB Life; 2019 Jul; 71(7):791-801. PubMed ID: 30746873
    [Abstract] [Full Text] [Related]

  • 5. Tafazzin Mutation Affecting Cardiolipin Leads to Increased Mitochondrial Superoxide Anions and Mitophagy Inhibition in Barth Syndrome.
    Petit PX, Ardilla-Osorio H, Penalvia L, Rainey NE.
    Cells; 2020 Oct 21; 9(10):. PubMed ID: 33096711
    [Abstract] [Full Text] [Related]

  • 6. Cardiolipin remodeling in Barth syndrome and other hereditary cardiomyopathies.
    Bertero E, Kutschka I, Maack C, Dudek J.
    Biochim Biophys Acta Mol Basis Dis; 2020 Aug 01; 1866(8):165803. PubMed ID: 32348916
    [Abstract] [Full Text] [Related]

  • 7. Barth Syndrome: Connecting Cardiolipin to Cardiomyopathy.
    Ikon N, Ryan RO.
    Lipids; 2017 Feb 01; 52(2):99-108. PubMed ID: 28070695
    [Abstract] [Full Text] [Related]

  • 8. Expression of human monolysocardiolipin acyltransferase-1 improves mitochondrial function in Barth syndrome lymphoblasts.
    Mejia EM, Zegallai H, Bouchard ED, Banerji V, Ravandi A, Hatch GM.
    J Biol Chem; 2018 May 18; 293(20):7564-7577. PubMed ID: 29563154
    [Abstract] [Full Text] [Related]

  • 9. Tafazzin deficiency impairs CoA-dependent oxidative metabolism in cardiac mitochondria.
    Le CH, Benage LG, Specht KS, Li Puma LC, Mulligan CM, Heuberger AL, Prenni JE, Claypool SM, Chatfield KC, Sparagna GC, Chicco AJ.
    J Biol Chem; 2020 Aug 28; 295(35):12485-12497. PubMed ID: 32665401
    [Abstract] [Full Text] [Related]

  • 10. Cardiac metabolic pathways affected in the mouse model of barth syndrome.
    Huang Y, Powers C, Madala SK, Greis KD, Haffey WD, Towbin JA, Purevjav E, Javadov S, Strauss AW, Khuchua Z.
    PLoS One; 2015 Aug 28; 10(6):e0128561. PubMed ID: 26030409
    [Abstract] [Full Text] [Related]

  • 11. Deficiency in Cardiolipin Reduces Doxorubicin-Induced Oxidative Stress and Mitochondrial Damage in Human B-Lymphocytes.
    Aryal B, Rao VA.
    PLoS One; 2016 Aug 28; 11(7):e0158376. PubMed ID: 27434059
    [Abstract] [Full Text] [Related]

  • 12. The functions of cardiolipin in cellular metabolism-potential modifiers of the Barth syndrome phenotype.
    Raja V, Greenberg ML.
    Chem Phys Lipids; 2014 Apr 28; 179():49-56. PubMed ID: 24445246
    [Abstract] [Full Text] [Related]

  • 13. The lipid environment modulates cardiolipin and phospholipid constitution in wild type and tafazzin-deficient cells.
    Oemer G, Koch J, Wohlfarter Y, Lackner K, Gebert REM, Geley S, Zschocke J, Keller MA.
    J Inherit Metab Dis; 2022 Jan 28; 45(1):38-50. PubMed ID: 34494285
    [Abstract] [Full Text] [Related]

  • 14. Mechano-energetic aspects of Barth syndrome.
    Dudek J, Maack C.
    J Inherit Metab Dis; 2022 Jan 28; 45(1):82-98. PubMed ID: 34423473
    [Abstract] [Full Text] [Related]

  • 15. Loss of tafazzin results in decreased myoblast differentiation in C2C12 cells: A myoblast model of Barth syndrome and cardiolipin deficiency.
    Lou W, Reynolds CA, Li Y, Liu J, Hüttemann M, Schlame M, Stevenson D, Strathdee D, Greenberg ML.
    Biochim Biophys Acta Mol Cell Biol Lipids; 2018 Aug 28; 1863(8):857-865. PubMed ID: 29694924
    [Abstract] [Full Text] [Related]

  • 16. Overexpression of mitochondrial oxodicarboxylate carrier (ODC1) preserves oxidative phosphorylation in a yeast model of Barth syndrome.
    de Taffin de Tilques M, Tribouillard-Tanvier D, Tétaud E, Testet E, di Rago JP, Lasserre JP.
    Dis Model Mech; 2017 Apr 01; 10(4):439-450. PubMed ID: 28188263
    [Abstract] [Full Text] [Related]

  • 17. Cardiolipin remodeling by TAZ/tafazzin is selectively required for the initiation of mitophagy.
    Hsu P, Liu X, Zhang J, Wang HG, Ye JM, Shi Y.
    Autophagy; 2015 Apr 03; 11(4):643-52. PubMed ID: 25919711
    [Abstract] [Full Text] [Related]

  • 18. TAZ encodes tafazzin, a transacylase essential for cardiolipin formation and central to the etiology of Barth syndrome.
    Garlid AO, Schaffer CT, Kim J, Bhatt H, Guevara-Gonzalez V, Ping P.
    Gene; 2020 Feb 05; 726():144148. PubMed ID: 31647997
    [Abstract] [Full Text] [Related]

  • 19. Experimental models of Barth syndrome.
    Pu WT.
    J Inherit Metab Dis; 2022 Jan 05; 45(1):72-81. PubMed ID: 34370877
    [Abstract] [Full Text] [Related]

  • 20. Barth syndrome cells display widespread remodeling of mitochondrial complexes without affecting metabolic flux distribution.
    Chatzispyrou IA, Guerrero-Castillo S, Held NM, Ruiter JPN, Denis SW, IJlst L, Wanders RJ, van Weeghel M, Ferdinandusse S, Vaz FM, Brandt U, Houtkooper RH.
    Biochim Biophys Acta Mol Basis Dis; 2018 Nov 05; 1864(11):3650-3658. PubMed ID: 30251684
    [Abstract] [Full Text] [Related]

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