Laura R Rodríguez, Pablo Calap-Quintana, Tamara Lapeña-Luzón, Federico V Pallardó, Stephan Schneuwly, Juan A Navarro, Pilar Gonzalez-Cabo. Redox Biol 2020
Times Cited: 14
Times Cited: 14
Times Cited
Times Co-cited
Similarity
Calcium Deregulation: Novel Insights to Understand Friedreich's Ataxia Pathophysiology.
Rosella Abeti, Alexander F Brown, Marta Maiolino, Sandip Patel, Paola Giunti. Front Cell Neurosci 2018
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Mitochondrial dysfunction induced by frataxin deficiency is associated with cellular senescence and abnormal calcium metabolism.
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Mitofusin 2 tethers endoplasmic reticulum to mitochondria.
Olga Martins de Brito, Luca Scorrano. Nature 2008
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Mitochondrial pore opening and loss of Ca2+ exchanger NCLX levels occur after frataxin depletion.
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Oxidative stress and altered lipid metabolism in Friedreich ataxia.
Jordi Tamarit, Èlia Obis, Joaquim Ros. Free Radic Biol Med 2016
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α-Synuclein binds to the ER-mitochondria tethering protein VAPB to disrupt Ca2+ homeostasis and mitochondrial ATP production.
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Altered interplay between endoplasmic reticulum and mitochondria in Charcot-Marie-Tooth type 2A neuropathy.
Nathalie Bernard-Marissal, Gerben van Hameren, Manisha Juneja, Christophe Pellegrino, Lauri Louhivuori, Luca Bartesaghi, Cylia Rochat, Omar El Mansour, Jean-Jacques Médard, Marie Croisier,[...]. Proc Natl Acad Sci U S A 2019
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Dysfunction in endoplasmic reticulum-mitochondria crosstalk underlies SIGMAR1 loss of function mediated motor neuron degeneration.
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ER-mitochondria tethering by PDZD8 regulates Ca2+ dynamics in mammalian neurons.
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Presenilin 2 Modulates Endoplasmic Reticulum-Mitochondria Coupling by Tuning the Antagonistic Effect of Mitofusin 2.
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α-Synuclein controls mitochondrial calcium homeostasis by enhancing endoplasmic reticulum-mitochondria interactions.
Tito Calì, Denis Ottolini, Alessandro Negro, Marisa Brini. J Biol Chem 2012
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Mitochondrial and endoplasmic reticulum calcium homeostasis and cell death.
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Modulation of the endoplasmic reticulum-mitochondria interface in Alzheimer's disease and related models.
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Mitochondria-Endoplasmic Reticulum Contacts in Reactive Astrocytes Promote Vascular Remodeling.
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ER tubules mark sites of mitochondrial division.
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SPLICS: a split green fluorescent protein-based contact site sensor for narrow and wide heterotypic organelle juxtaposition.
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Redox Nanodomains Are Induced by and Control Calcium Signaling at the ER-Mitochondrial Interface.
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Mitochondria-associated endoplasmic reticulum membrane (MAM) integrity is required for insulin signaling and is implicated in hepatic insulin resistance.
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Apoptotic cell death and altered calcium homeostasis caused by frataxin depletion in dorsal root ganglia neurons can be prevented by BH4 domain of Bcl-xL protein.
Stefka Mincheva-Tasheva, Elia Obis, Jordi Tamarit, Joaquim Ros. Hum Mol Genet 2014
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Gene Transfer of Brain-derived Neurotrophic Factor (BDNF) Prevents Neurodegeneration Triggered by FXN Deficiency.
Yurika Katsu-Jiménez, Frida Loría, Juan Carlos Corona, Javier Díaz-Nido. Mol Ther 2016
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Metabolic remodeling in frataxin-deficient yeast is mediated by Cth2 and Adr1.
Armando Moreno-Cermeño, David Alsina, Elisa Cabiscol, Jordi Tamarit, Joaquim Ros. Biochim Biophys Acta 2013
Armando Moreno-Cermeño, David Alsina, Elisa Cabiscol, Jordi Tamarit, Joaquim Ros. Biochim Biophys Acta 2013
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Manganese is the link between frataxin and iron-sulfur deficiency in the yeast model of Friedreich ataxia.
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14
Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia.
Elena Britti, Fabien Delaspre, A Sanz-Alcázar, Marta Medina-Carbonero, Marta Llovera, Rosa Purroy, Stefka Mincheva-Tasheva, Jordi Tamarit, Joaquim Ros. Biochem J 2021
Elena Britti, Fabien Delaspre, A Sanz-Alcázar, Marta Medina-Carbonero, Marta Llovera, Rosa Purroy, Stefka Mincheva-Tasheva, Jordi Tamarit, Joaquim Ros. Biochem J 2021
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Frataxin-deficient cardiomyocytes present an altered thiol-redox state which targets actin and pyruvate dehydrogenase.
Rosa Purroy, Marta Medina-Carbonero, Joaquim Ros, Jordi Tamarit. Redox Biol 2020
Rosa Purroy, Marta Medina-Carbonero, Joaquim Ros, Jordi Tamarit. Redox Biol 2020
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Iron regulatory protein-1 and -2: transcriptome-wide definition of binding mRNAs and shaping of the cellular proteome by iron regulatory proteins.
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Mitochondrial iron detoxification is a primary function of frataxin that limits oxidative damage and preserves cell longevity.
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PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia.
Laura Rodríguez-Pascau, Elena Britti, Pablo Calap-Quintana, Yi Na Dong, Cristina Vergara, Fabien Delaspre, Marta Medina-Carbonero, Jordi Tamarit, Federico V Pallardó, Pilar Gonzalez-Cabo,[...]. Neurobiol Dis 2021
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Aconitase and mitochondrial iron-sulphur protein deficiency in Friedreich ataxia.
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Loss of Frataxin induces iron toxicity, sphingolipid synthesis, and Pdk1/Mef2 activation, leading to neurodegeneration.
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GRP75 overexpression rescues frataxin deficiency and mitochondrial phenotypes in Friedreich ataxia cellular models.
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PKA Phosphorylation of NCLX Reverses Mitochondrial Calcium Overload and Depolarization, Promoting Survival of PINK1-Deficient Dopaminergic Neurons.
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Ferroptosis as a Novel Therapeutic Target for Friedreich's Ataxia.
M Grazia Cotticelli, Shujuan Xia, Daniel Lin, Taehee Lee, Leila Terrab, Peter Wipf, Donna M Huryn, Robert B Wilson. J Pharmacol Exp Ther 2019
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Yeast frataxin mutants display decreased superoxide dismutase activity crucial to promote protein oxidative damage.
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Actin glutathionylation increases in fibroblasts of patients with Friedreich's ataxia: a potential role in the pathogenesis of the disease.
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Mechanism of activation of the human cysteine desulfurase complex by frataxin.
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Iron in Friedreich Ataxia: A Central Role in the Pathophysiology or an Epiphenomenon?
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α-Synuclein emerges as a potent regulator of VDAC-facilitated calcium transport.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.