Michael E. Baumgartner
University of Bristol
6 Papers
8 Citations
Michael E. Baumgartner is an academic researcher from University of Bristol. The author has contributed to research in topics: Proteostasis & Induced pluripotent stem cell. The author has an hindex of 1, co-authored 6 publications.
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Papers
Proteotoxic stress is a driver of the loser status and cell competition.
TL;DR: In this article, the authors show that reduced translation does not cause cell competition and instead, proteotoxic stress is the underlying cause of the loser status for minute competition and competition induced by mahjong, an unrelated loser gene.
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Progenitor cell therapy for acquired pediatric nervous system injury: Traumatic brain injury and acquired sensorineural hearing loss.
James E. Baumgartner,Linda S. Baumgartner,Michael E. Baumgartner,Ernest J. Moore,Steven A. Messina,Michael D. Seidman,David Shook +6 more
TL;DR: It is suggested that multipotent stem cell therapies achieve therapeutic effect by altering the immune response to injury, thereby limiting damage due to inflammation and possibly promoting repair.
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Ribosome protein mutant cells rely on the GR64 cluster of gustatory receptors for survival and proteostasis in Drosophila
TL;DR: The authors showed that Rp/+ cells depend on Gr64 for survival and that loss of Gr64 autonomously exacerbates stress pathway activation and proteotoxic stress by negatively affecting autophagy and proteasome function in Rp+ cells.
PECAn, a pipeline for image processing and statistical analysis of complex mosaic 3D tissues
TL;DR: In this paper, a pipeline for image processing and statistical data analysis is developed to automatically extract sophisticated parameters from complex multi-genotype 3D images, including data handling, machine-learning-enabled segmentation, multivariant statistical analysis, and graph generation.
Xrp1 and Irbp18 trigger a feed-forward loop of proteotoxic stress to induce the loser status
TL;DR: In this article, the authors show that Xrp1 is necessary for Rp/+ -induced proteotoxic stress and is sufficient to induce proteotic stress in otherwise wild-type cells.