M
Michael Sendtner
Researcher at University of Würzburg
Publications - 286
Citations - 34780
Michael Sendtner is an academic researcher from University of Würzburg. The author has contributed to research in topics: Ciliary neurotrophic factor & Neurotrophic factors. The author has an hindex of 88, co-authored 269 publications receiving 31409 citations. Previous affiliations of Michael Sendtner include Hoffmann-La Roche & Regeneron.
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Differential modulation of neurite growth by the S- and the L-forms of bag1, a co-chaperone of Hsp70.
TL;DR: Data indicate that the cytosolic form of bag1 participates in neurotrophin-mediated neurite growth, and that interaction with Hsp70 plays a crucial role in this context.
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Spiral Ganglion Outgrowth and Hearing Development in p75NTR-Deficient Mice
D. Brors,Stefan Hansen,Robert Mlynski,Stefan Volkenstein,Christoph Aletsee,Michael Sendtner,Allen F. Ryan,Stefan Dazert +7 more
TL;DR: P75NTR has a remarkable influence on spiral ganglion neurite growth behavior, but it does not seem to be essential for the development of basic hearing function in the first 3 postnatal weeks.
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Analysis of European case-control studies suggests that common inherited variation in mitochondrial DNA is not involved in susceptibility to amyotrophic lateral sclerosis
Catherine J. E. Ingram,Michael E. Weale,Christopher A Plaster,Karen E. Morrison,Emily F. Goodall,Hardev Pall,Marcus Beck,Sibylle Jablonka,Michael Sendtner,Elizabeth M. C. Fisher,Neil Bradman,Dalia Kasperavičiūtė +11 more
TL;DR: It is unlikely that common, shared genetic variants in the mitochondrial genome contribute substantially to ALS, using an economic and efficient method to test whether such involvement is probable.
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Overexpression of an ALS-associated FUS mutation in C. elegans disrupts NMJ morphology and leads to defective neuromuscular transmission.
Sebastian M. Markert,Michael Peter Skoruppa,Bin Yu,Ben Mulcahy,Mei Zhen,Mei Zhen,Shangbang Gao,Michael Sendtner,Christian Stigloher +8 more
TL;DR: It is shown that ectopic expression of wild-type or ALS-associated human FUS impairs synaptic vesicle docking at neuromuscular junctions, and this suggests a pathological effect of ALS-causing FUS at synaptic structure and function organization.
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Damaging secretions: chromogranins team up with mutant SOD1.
TL;DR: A familial form of ALS is caused by mutations in the superoxide dismutase (SOD1) gene and a new paper shows that mutant SOD1 binds chromogranins in secretory vesicles and that its release promotes microgliosis and motor neuron death.