Tobias M. Boeckers, MD
Affiliations: | University of Ulm, Ulm, Baden-Württemberg, Germany |
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"Tobias Boeckers"Mean distance: 16.67 (cluster 32) | S | N | B | C | P |
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Sign in to add mentorEckart D. Gundelfinger | research scientist | Leibniz Institute for Neurobiology |
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Publications
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Giona F, Beretta S, Zippo A, et al. (2025) Shank3 modulates Rpl3 expression and protein synthesis via mGlu5: implications for Phelan McDermid syndrome. Molecular Psychiatry |
Vinci E, Beretta S, Colombo V, et al. (2025) Regulation of Dendrite and Dendritic Spine Formation by TCF20. Journal of Neurochemistry. 169: e16297 |
Lehmann J, Aly A, Steffke C, et al. (2024) Heterozygous knockout of Synaptotagmin13 phenocopies ALS features and TP53 activation in human motor neurons. Cell Death & Disease. 15: 560 |
Delling JP, Bauer HF, Gerlach-Arbeiter S, et al. (2024) Combined expansion and STED microscopy reveals altered fingerprints of postsynaptic nanostructure across brain regions in ASD-related SHANK3-deficiency. Molecular Psychiatry |
Aly A, Laszlo ZI, Rajkumar S, et al. (2023) Correction to: Integrative proteomics highlight presynaptic alterations and c-Jun misactivation as convergent pathomechanisms in ALS. Acta Neuropathologica |
Seidel M, Rajkumar S, Steffke C, et al. (2023) Propranolol reduces the accumulation of cytotoxic aggregates in C9orf72-ALS/FTD models. Current Research in Neurobiology. 5: 100105 |
Aly A, Laszlo ZI, Rajkumar S, et al. (2023) Integrative proteomics highlight presynaptic alterations and c-Jun misactivation as convergent pathomechanisms in ALS. Acta Neuropathologica |
Catanese A, Rajkumar S, Sommer D, et al. (2023) Multiomics and machine-learning identify novel transcriptional and mutational signatures in amyotrophic lateral sclerosis. Brain : a Journal of Neurology |
Sommer D, Rajkumar S, Seidel M, et al. (2022) Aging-Dependent Altered Transcriptional Programs Underlie Activity Impairments in Human C9orf72-Mutant Motor Neurons. Frontiers in Molecular Neuroscience. 15: 894230 |
Urrutia-Ruiz C, Rombach D, Cursano S, et al. (2022) Deletion of the Autism-Associated Protein SHANK3 Abolishes Structural Synaptic Plasticity after Brain Trauma. International Journal of Molecular Sciences. 23 |