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Edward T. W. Bampton

Researcher at University of Leicester

Publications -  14
Citations -  5480

Edward T. W. Bampton is an academic researcher from University of Leicester. The author has contributed to research in topics: Endoplasmic reticulum & Apoptosis. The author has an hindex of 11, co-authored 14 publications receiving 4473 citations. Previous affiliations of Edward T. W. Bampton include University of Cambridge.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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The dynamics of autophagy visualized in live cells: from autophagosome formation to fusion with endo/lysosomes.

TL;DR: Use of fluorescent LC3 and a counterfluorescent endosomal/lysosomal protein clearly allows the entire autophagic process to be followed by live cell imaging with high fidelity, and reveals novel insights into the dynamics of autophagosome homeostasis.
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The in vitro cleavage of the hAtg proteins by cell death proteases

TL;DR: It is shown that the majority of human Atg proteins can be cleaved by calpain 1, which is activated in some apoptotic paradigms, as well as other forms of death, and that p62 is a target for caspase-6 and -8 cleavage.
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BCL2/BCL-X(L) inhibition induces apoptosis, disrupts cellular calcium homeostasis, and prevents platelet activation.

TL;DR: It is shown, for the first time, that these BCL2/BCL-X(L) inhibitors do not offer any selective toxicity but induce apoptosis at similar concentrations in leukemia cells and platelets, however, reticulated platelets are less sensitive to apoptosis, supporting the hypothesis that treatment with ABT-263 induces a selective loss of older platelets and providing an explanation for the transient thrombocytopenia observed on ABt-263 treatment.
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Hyperglycaemia inhibits Schwann cell proliferation and migration and restricts regeneration of axons and Schwann cells from adult murine DRG

TL;DR: SC proliferation and migration, and axon regeneration from DRG neurons, are impaired by hyperglycaemia cell autonomously, while apoptosis is negligible, and impairment of these functions over time may exacerbate nerve injury-related diabetic neuropathy.