| AMPK stimulation inhibits YAP/TAZ signaling to ameliorate hepatic fibrosis. | AMPK stimulation inhibits YAP/TAZ signaling to ameliorate hepatic fibrosis.
Shihan MH, Sharma S, Cable C, Prathigudupu V, Chen A, Mattis AN, Chen JY., Free PMC Article | 03/6/2024 |
| YAP and TAZ regulate remyelination in the central nervous system. | YAP and TAZ regulate remyelination in the central nervous system.
Hong J, Kirkland JM, Acheta J, Marziali LN, Beck B, Jeanette H, Bhatia U, Davis G, Herron J, Roué C, Abi-Ghanem C, Feltri ML, Zuloaga KL, Bechler ME, Poitelon Y, Belin S., | 11/14/2023 |
| Elabela-APJ axis mediates angiogenesis via YAP/TAZ pathway in cerebral ischemia/reperfusion injury. | Elabela-APJ axis mediates angiogenesis via YAP/TAZ pathway in cerebral ischemia/reperfusion injury.
Li W, Xu P, Kong L, Feng S, Shen N, Huang H, Wang W, Xu X, Wang X, Wang G, Zhang Y, Sun W, Hu W, Liu X. | 05/17/2023 |
| Mice Deficient in TAZ (Wwtr1) Demonstrate Clinical Features of Late-Onset Fuchs' Endothelial Corneal Dystrophy. | Mice Deficient in TAZ (Wwtr1) Demonstrate Clinical Features of Late-Onset Fuchs' Endothelial Corneal Dystrophy.
Leonard BC, Park S, Kim S, Young LJ, Jalilian I, Cosert K, Zhang X, Skeie JM, Shevalye H, Echeverria N, Rozo V, Gong X, Xing C, Murphy CJ, Greiner MA, Mootha VV, Raghunathan VK, Thomasy SM., Free PMC Article | 04/21/2023 |
| Tafazzin deficiency attenuates anti-cluster of differentiation 40 and interleukin-4 activation of mouse B lymphocytes. | Tafazzin deficiency attenuates anti-cluster of differentiation 40 and interleukin-4 activation of mouse B lymphocytes.
Zegallai HM, Abu-El-Rub E, Mejia EM, Sparagna GC, Cole LK, Marshall AJ, Hatch GM. | 12/17/2022 |
| Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes. | Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.
Zegallai HM, Abu-El-Rub E, Olayinka-Adefemi F, Cole LK, Sparagna GC, Marshall AJ, Hatch GM. | 07/16/2022 |
| A new murine model of Barth syndrome neutropenia links TAFAZZIN deficiency to increased ER stress-induced apoptosis. | A new murine model of Barth syndrome neutropenia links TAFAZZIN deficiency to increased ER stress-induced apoptosis.
Sohn J, Milosevic J, Brouse T, Aziz N, Elkhoury J, Wang S, Hauschild A, van Gastel N, Cetinbas M, Tufa SF, Keene DR, Sadreyev RI, Pu WT, Sykes DB., Free PMC Article | 04/30/2022 |
| Tafazzin Modulates Allergen-Induced Mast Cell Inflammatory Mediator Secretion. | Tafazzin Modulates Allergen-Induced Mast Cell Inflammatory Mediator Secretion.
Maguire ARR, Crozier RWE, Hunter KD, Claypool SM, Fajardo VA, LeBlanc PJ, MacNeil AJ. | 02/5/2022 |
| Tafazzin deficiency impairs mitochondrial metabolism and function of lipopolysaccharide activated B lymphocytes in mice. | Tafazzin deficiency impairs mitochondrial metabolism and function of lipopolysaccharide activated B lymphocytes in mice.
Zegallai HM, Abu-El-Rub E, Cole LK, Field J, Mejia EM, Gordon JW, Marshall AJ, Hatch GM. | 12/25/2021 |
| Tafazzin Deficiency Reduces Basal Insulin Secretion and Mitochondrial Function in Pancreatic Islets From Male Mice. | Tafazzin Deficiency Reduces Basal Insulin Secretion and Mitochondrial Function in Pancreatic Islets From Male Mice.
Cole LK, Agarwal P, Doucette CA, Fonseca M, Xiang B, Sparagna GC, Seshadri N, Vandel M, Dolinsky VW, Hatch GM., Free PMC Article | 10/9/2021 |
| A mouse model of short-term, diet-induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression. | A mouse model of short-term, diet-induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression.
Sakurai T, Chen Z, Yamahata A, Hayasaka T, Satoh H, Sekiguchi H, Chiba H, Hui SP. | 08/14/2021 |
| Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide/H2 O2 production in heart and skeletal muscle mitochondria. | Cardiolipin deficiency in Barth syndrome is not associated with increased superoxide/H(2) O(2) production in heart and skeletal muscle mitochondria.
Goncalves RLS, Schlame M, Bartelt A, Brand MD, Hotamışlıgil GS., Free PMC Article | 07/31/2021 |
| Tafazzin deficiency impairs CoA-dependent oxidative metabolism in cardiac mitochondria. | 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., Free PMC Article | 01/23/2021 |
| AAV-Mediated TAZ Gene Replacement Restores Mitochondrial and Cardioskeletal Function in Barth Syndrome. | AAV-Mediated TAZ Gene Replacement Restores Mitochondrial and Cardioskeletal Function in Barth Syndrome.
Suzuki-Hatano S, Saha M, Rizzo SA, Witko RL, Gosiker BJ, Ramanathan M, Soustek MS, Jones MD, Kang PB, Byrne BJ, Cade WT, Pacak CA., Free PMC Article | 03/14/2020 |
| Tafazzin-deficient mice hearts display reduced HIF-1alpha levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. | Defective Mitochondrial Cardiolipin Remodeling Dampens HIF-1α Expression in Hypoxia.
Chowdhury A, Aich A, Jain G, Wozny K, Lüchtenborg C, Hartmann M, Bernhard O, Balleiniger M, Alfar EA, Zieseniss A, Toischer K, Guan K, Rizzoli SO, Brügger B, Fischer A, Katschinski DM, Rehling P, Dudek J., Free PMC Article | 12/14/2019 |
| in vitro studies demonstrate that mitochondria-targeted antioxidants improve contractile capacity in TAZ-deficient cardiomyocytes. The purpose of the present study was to determine if resolving mitochondrial oxidative stress would be sufficient to prevent cardiomyopathy and skeletal myopathy in vivo using a mouse model of Barth Syndrome | Targeted overexpression of catalase to mitochondria does not prevent cardioskeletal myopathy in Barth syndrome.
Johnson JM, Ferrara PJ, Verkerke ARP, Coleman CB, Wentzler EJ, Neufer PD, Kew KA, de Castro Brás LE, Funai K., Free PMC Article | 09/28/2019 |
| Tafazzin was elevated in the hearts of high-fat-diet fed mice.Increased tafazzin contributes to insulin resistance via mediating Drp-1 translocation to the mitochondria. | Increased Dynamin-Related Protein 1-Dependent Mitochondrial Fission Contributes to High-Fat-Diet-Induced Cardiac Dysfunction and Insulin Resistance by Elevating Tafazzin in Mouse Hearts.
Chang W, Xiao D, Ao X, Li M, Xu T, Wang J. | 09/21/2019 |
| Findings demonstrate that TAZ-mediated remodeling of cardiolipin (CL) contributes significantly to the expansive distribution of CL molecular species in the brain, plays a key role in mitochondria respiratory activity, maintains normal cognitive function. | Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice.
Cole LK, Kim JH, Amoscato AA, Tyurina YY, Bay R H, Karimi B, Siddiqui TJ, Kagan VE, Hatch GM, Kauppinen TM., Free PMC Article | 05/25/2019 |
| targeting mTORC2 retards fibroblast activation and kidney fibrosis through suppressing Yap/Taz activation. | Yap/Taz mediates mTORC2-stimulated fibroblast activation and kidney fibrosis.
Gui Y, Li J, Lu Q, Feng Y, Wang M, He W, Yang J, Dai C., Free PMC Article | 03/23/2019 |
| results suggest that plasmenylcholine, abundant in linoleoyl species, is important in remodeling CL in the heart. Tafazzin deficiency thus has a major impact on the cardiac plasmenylcholine level and thereby its functions. | Substantial Decrease in Plasmalogen in the Heart Associated with Tafazzin Deficiency.
Kimura T, Kimura AK, Ren M, Berno B, Xu Y, Schlame M, Epand RM., Free PMC Article | 05/12/2018 |
| The impact of endurance training on the cardiac and skeletal muscle phenotype in young TAZ knock-down mice. | Endurance training ameliorates complex 3 deficiency in a mouse model of Barth syndrome.
Soustek MS, Baligand C, Falk DJ, Walter GA, Lewin AS, Byrne BJ. | 07/16/2016 |
| impaired Taz-function with onset at adult age does not enhance susceptibility to ischemia-reperfusion injury. | Acquired deficiency of tafazzin in the adult heart: Impact on mitochondrial function and response to cardiac injury.
Szczepanek K, Allegood J, Aluri H, Hu Y, Chen Q, Lesnefsky EJ. | 06/11/2016 |
| A novel role for Taz in helping to maintain genome integrity in spermatocyte meiosis and facilitating germ cell differentiation. | Mouse Tafazzin Is Required for Male Germ Cell Meiosis and Spermatogenesis.
Cadalbert LC, Ghaffar FN, Stevenson D, Bryson S, Vaz FM, Gottlieb E, Strathdee D., Free PMC Article | 04/30/2016 |
| Tafazzin deficiency in mouse embryonic fibroblasts also led to impaired oxidative phosphorylation and severe oxidative stress | 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., Free PMC Article | 03/19/2016 |
| TAZ mutation is necessary and sufficient for the phenotype of sparse and irregular sarcomeres and weak myocaridal contraction foudn in Barth syndrome. | Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies.
Wang G, McCain ML, Yang L, He A, Pasqualini FS, Agarwal A, Yuan H, Jiang D, Zhang D, Zangi L, Geva J, Roberts AE, Ma Q, Ding J, Chen J, Wang DZ, Li K, Wang J, Wanders RJ, Kulik W, Vaz FM, Laflamme MA, Murry CE, Chien KR, Kelley RI, Church GM, Parker KK, Pu WT., Free PMC Article | 09/27/2014 |