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Full-Text Articles in Life Sciences
Wilms Tumor 1b Defines A Wound-Specific Sheath Cell Subpopulation Associated With Notochord Repair, Juan Carlos Lopez-Baez, Daniel J. Simpson, Laura Lleras Forero, Zhiqiang Zeng, Hannah Brunsdon, Angela Salzano, Alessandro Brombin, Cameron Wyatt, Witold Rybski, Leonie F A Huitema, Rodney M. Dale, Koichi Kawakami, Christoph Englert, Tamir Chandra, Stefan Schulte-Merker, Nicholas D. Hastie, E Elizabeth Patton
Wilms Tumor 1b Defines A Wound-Specific Sheath Cell Subpopulation Associated With Notochord Repair, Juan Carlos Lopez-Baez, Daniel J. Simpson, Laura Lleras Forero, Zhiqiang Zeng, Hannah Brunsdon, Angela Salzano, Alessandro Brombin, Cameron Wyatt, Witold Rybski, Leonie F A Huitema, Rodney M. Dale, Koichi Kawakami, Christoph Englert, Tamir Chandra, Stefan Schulte-Merker, Nicholas D. Hastie, E Elizabeth Patton
Biology: Faculty Publications and Other Works
Regenerative therapy for degenerative spine disorders requires the identification of cells that can slow down and possibly reverse degenerative processes. Here, we identify an unanticipated wound-specific notochord sheath cell subpopulation that expresses Wilms Tumor (WT) 1b following injury in zebrafish. We show that localized damage leads to Wt1b expression in sheath cells, and that wt1b+cells migrate into the wound to form a stopper-like structure, likely to maintain structural integrity. Wt1b+sheath cells are distinct in expressing cartilage and vacuolar genes, and in repressing a Wt1b-p53 transcriptional programme. At the wound, wt1b+and entpd5+ cells constitute …
Investigating Autophagy, Extracellular Vesicles, And Glycobiology, Benjamin Cook
Investigating Autophagy, Extracellular Vesicles, And Glycobiology, Benjamin Cook
Master's Theses
Autophagy is a cellular process of degradation which degrades cellular materials in acidic organelles called lysosomes. Impairment of lysosomal degradation can lead to lysosomal storage disorders such as Parkinson's Disease. In Parkinson's Disease neurotoxic α-synuclein can spread from cell-to-cell via extracellular vesicles. We investigated the changes in extra vesicular glycans upon perturbation of autophagy using a class of glycan binding molecules termed lectins.
We found that upon induction of autophagy causes EV glycans to increase while others remained consistent. Additionally, we found that specific glycans are increased more than others. Conversely, when lysosomal degradation was impaired, we observed a decrease …