Zobrazeno 1 - 10
of 21
pro vyhledávání: '"Sendtner, Michael"'
Autor:
Jandke, Solveig, Garz, Cornelia, Schwanke, Daniel, Sendtner, Michael, Heinze, Hans-Jochen, Carare, Roxana O, Schreiber, Stefanie
Publikováno v:
Brain Pathology
Brain pathology 28(6), 844-859 (2018). doi:10.1111/bpa.12629
Brain pathology 28(6), 844-859 (2018). doi:10.1111/bpa.12629
We aimed to test the hypothesis that in spontaneously hypertensive stroke‐prone rats (SHRSP), non‐amyloid cerebral small vessel disease/hypertensive arteriopathy (HA) results in vessel wall injury that may promote cerebral amyloid angiopathy (CAA
Autor:
Ghanawi, Hanaa, Hennlein, Luisa, Zare, Abdolhossein, Bader, Jakob, Salehi, Saeede, Hornburg, Daniel, Ji, Changhe, Sivadasan, Rajeeve, Drepper, Carsten, Meissner, Felix, Mann, Matthias, Jablonka, Sibylle, Briese, Michael, Sendtner, Michael
Publikováno v:
Nucleic Acids Research
Ghanawi, H, Hennlein, L, Zare, A, Bader, J, Salehi, S, Hornburg, D, Ji, C, Sivadasan, R, Drepper, C, Meissner, F, Mann, M, Jablonka, S, Briese, M & Sendtner, M 2021, ' Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin ', Nucleic Acids Symposium Series, vol. 49, no. 21, pp. 12284-12305 . https://doi.org/10.1093/nar/gkab1120
Ghanawi, H, Hennlein, L, Zare, A, Bader, J, Salehi, S, Hornburg, D, Ji, C, Sivadasan, R, Drepper, C, Meissner, F, Mann, M, Jablonka, S, Briese, M & Sendtner, M 2021, ' Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin ', Nucleic Acids Symposium Series, vol. 49, no. 21, pp. 12284-12305 . https://doi.org/10.1093/nar/gkab1120
Neurons critically rely on the functions of RNA-binding proteins to maintain their polarity and resistance to neurotoxic stress. HnRNP R has a diverse range of post-transcriptional regulatory functions and is important for neuronal development by reg
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::2171229b8598fec939158b4716daa015
https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-265687
https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-265687
Introduction: Deep brain stimulation is an established method for the treatment of neurological and psychiatric disorders. To elicit the underlying mechanisms and explore new stimulation targets, rodent models are necessary. Cable bound external stim
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::13688154185311363852e13e67dcebe7
https://duepublico2.uni-due.de/servlets/MCRFileNodeServlet/duepublico_derivate_00073497/Fleischer_et_al_fnins-14-00726.pdf
https://duepublico2.uni-due.de/servlets/MCRFileNodeServlet/duepublico_derivate_00073497/Fleischer_et_al_fnins-14-00726.pdf
Autor:
Briese, Michael, Saal-Bauernschubert, Lena, Lüningschrör, Patrick, Moradi, Mehri, Dombert, Benjamin, Surrey, Verena, Appenzeller, Silke, Deng, Chunchu, Jablonka, Sibylle, Sendtner, Michael
Publikováno v:
Acta Neuropathologica Communications
Acta Neuropathologica Communications, Vol 8, Iss 1, Pp 1-16 (2020)
Acta Neuropathologica Communications, Vol 8, Iss 1, Pp 1-16 (2020)
Protein inclusions containing the RNA-binding protein TDP-43 are a pathological hallmark of amyotrophic lateral sclerosis and other neurodegenerative disorders. The loss of TDP-43 function that is associated with these inclusions affects post-transcr
Autor:
Lüningschrör, Patrick, Slotta, Carsten, Heimann, Peter, Briese, Michael, Weikert, Ulrich, Massih, Bita, Appenzeller, Silke, Sendtner, Michael, Kaltschmidt, Christian, Kaltschmidt, Barbara
Publikováno v:
Frontiers in Cellular Neuroscience
Inflammation and dysregulation of the immune system are hallmarks of several neurodegenerative diseases. An activated immune response is considered to be the cause of myelin breakdown in demyelinating disorders. In the peripheral nervous system (PNS)
Autor:
Müller, Kathrin, Brenner, David, Kubisch, Christian, Klopstock, Thomas, Zeller, Daniel, Jablonka, Sibylle, Sendtner, Michael, Klebe, Stephan, Knehr, Antje, Günther, Kornelia, Weis, Joachim, Claeys, Kristl G, Weydt, Patrick, Schrank, Berthold, Sperfeld, Anne-Dorte, Hübers, Annemarie, Otto, Markus, Dorst, Johannes, Meitinger, Thomas, Strom, Tim M, Andersen, Peter M, Ludolph, Albert, Weishaupt, Jochen H, Meyer, Thomas, MND-NET, German ALS network, Weyen, Ute, Hermann, Andreas, Regensburger, Martin, Winkler, Jürgen, Linker, Ralf, Winner, Beate, Hagenacker, Tim, Koch, Jan Christoph, Lingor, Paul, Grehl, Torsten, Göricke, Bettina, Zierz, Stephan, Jordan, Berit, Baum, Petra, Wolf, Joachim, Winkler, Andrea, Young, Peter, Bogdahn, Ulrich, Prudlo, Johannes, Kassubek, Jan, Petri, Susanne, Danzer, Karin M, Grosskreutz, Julian, Schuster, Joachim, Volk, Alexander E, Borck, Guntram
Publikováno v:
Journal of neurology, neurosurgery, and psychiatry 89(8), 817-827 (2018). doi:10.1136/jnnp-2017-317611
Journal of Neurology, Neurosurgery, and Psychiatry
J. Neurol. Neurosurg. Psychiatr. 89, 817-827 (2018)
Journal of Neurology, Neurosurgery, and Psychiatry
J. Neurol. Neurosurg. Psychiatr. 89, 817-827 (2018)
ObjectivesRecent advances in amyotrophic lateral sclerosis (ALS) genetics have revealed that mutations in any of more than 25 genes can cause ALS, mostly as an autosomal-dominant Mendelian trait. Detailed knowledge about the genetic architecture of A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbbb9591c55245bd90ac99345f5b547b
https://pub.dzne.de/record/140154
https://pub.dzne.de/record/140154
Autor:
Brenner, David, Yilmaz, Rüstem, Weber, Markus, Pinto, Susana, Claeys, Kristl, Schrank, Berthold, Jordan, Berit, Knehr, Antje, Günther, Kornelia, Hübers, Annemarie, Zeller, Daniel, Kubisch, Christian, Müller, Kathrin, Jablonka, Sibylle, Sendtner, Michael, Klopstock, Thomas, de Carvalho, Mamede, Sperfeld, Anne, Borck, Guntram, Volk, Alexander E., Dorst, Johannes, Weis, Joachim, Otto, Markus, Grehl, Torsten, Schuster, Joachim, Del Tredici, Kelly, Braak, Heiko, Danzer, Karin M., Freischmidt, Axel, Meitinger, Thomas, Strom, Tim M., Ludolph, Albert C., Andersen, Peter M., Weishaupt, Jochen H., Petri, Susanne, German ALS network MND-NET, Weyen, Ute, Hermann, Andreas, Hagenacker, Tim, Koch, Jan Christoph, Lingor, Paul, Göricke, Bettina, Zierz, Stephan, Baum, Petra, Wolf, Joachim, Meyer, Thomas, Winkler, Andrea, Young, Peter, Bogdahn, Ulrich, Prudlo, Johannes, Kassubek, Jan, Grosskreutz, Julian, Weydt, Patrick, Ruf, Wolfgang, Neuwirth, Christoph
Publikováno v:
Brain : a journal of neurology 141(3), 688-697 (2018). doi:10.1093/brain/awx370
Brain
PubMed Central
Publikationer från Umeå universitet
OpenAIRE
Lirias
Brain 141(3), 688-697 (2018). doi:10.1093/brain/awx370
Brain
PubMed Central
Publikationer från Umeå universitet
OpenAIRE
Lirias
Brain 141(3), 688-697 (2018). doi:10.1093/brain/awx370
Brenner et al. show that mutations in a C-terminal hotspot of kinesin-5A (KIF5A) can cause a classical ALS phenotype. Experiments using patient-derived cell lines suggest haploinsufficiency as the molecular genetic mechanism. This underlines the rele
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c3f40d2dcee1873508c7948349c21d0
https://lirias.kuleuven.be/handle/123456789/611026
https://lirias.kuleuven.be/handle/123456789/611026
Autor:
Sendtner, Michael, Thoenen, Hans
Transgenic mice carrying mutated Cu/Zn superoxide dismutase genes provide insights into the pathogenesis of human motorneuron diseases and may be useful as models in the development and testing of therapies.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=od_______713::72a4fcbeb0c3a118de9af2d0b634056d
https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/3590
https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/3590
Autor:
Lütticken, Claudia, Wegenka, Ursula M., Yuan, Juping, Buschmann, Jan, Schindler, Chris, Ziemiecki, Andrew, Harpur, Alisa G., Wilks, Andrew F., Yasukawa, Kiyoshi, Taga, Tetsuya, Kishimoto, Tadamitsu, Barbieri, Giovanna, Sendtner, Michael, Pellegrini, Sandra, Heinrich, Peter C., Horn, Friedemann
Interleukin-6, leukemia inhibitory factor, oncostatin M. Interleukin-11, and cilialy neurotrophic factor bind to receptor complexes that share the signal transducer gp130. Upon binding, the ligands rapidly activate DNA binding of acute-phase response
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=od_______713::a3986ff67ac36871941a66d9a344e909
https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/3611
https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/3611