Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration von Gispert, Suzana, Ricciardi, Filomena, Kurz, Alexander, Azizov, Mekhman, Hoepken, Hans-Hermann, Becker, Dorothea, Voos, Wolfgang, Leuner, Kristina, Müller, Walter E, Kudin, Alexei P, Kunz, Wolfram S, Zimmermann, Annabelle, Roeper, Jochen, Wenzel, Dirk, Jendrach, Marina, García-Arencíbia, Moisés, Fernández-Ruiz, Javier, Huber, Leslie, Rohrer, Hermann, Barrera, Miguel, Reichert, Andreas S, Rüb, Udo, Chen, Amy, Nussbaum, Robert L, Auburger, Georg

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ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice von Damrath, Ewa, Heck, Melanie V, Gispert, Suzana, Azizov, Mekhman, Nowock, Joachim, Seifried, Carola, Rüb, Udo, Walter, Michael, Auburger, Georg

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Dysregulated expression of lipid storage and membrane dynamics factors in Tia1 knockout mouse nervous tissue von Heck, Melanie Vanessa, Azizov, Mekhman, Stehning, Tanja, Walter, Michael, Kedersha, Nancy, Auburger, Georg

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Insulin receptor and lipid metabolism pathology in ataxin-2 knock-out mice von Lastres-Becker, Isabel, Brodesser, Susanne, Lütjohann, Dieter, Azizov, Mekhman, Buchmann, Jana, Hintermann, Edith, Sandhoff, Konrad, Schürmann, Annette, Nowock, Joachim, Auburger, Georg

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Parkinson patient fibroblasts show increased alpha-synuclein expression von Hoepken, Hans-Hermann, Gispert, Suzana, Azizov, Mekhman, Klinkenberg, Michael, Ricciardi, Filomena, Kurz, Alexander, Morales-Gordo, Blas, Bonin, Michael, Riess, Olaf, Gasser, Thomas, Kögel, Donat, Steinmetz, Helmuth, Auburger, Georg

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Genetic ablation of ataxin-2 increases several global translation factors in their transcript abundance but decreases translation rate von Fittschen, Monica

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Dysregulated expression of lipid storage and membrane dynamics factors in Tia1 knockout mouse nervous tissue von Heck, Melanie Vanessa

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ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice

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Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration

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