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Kimberly McCall

Researcher at Boston University

Publications -  56
Citations -  9724

Kimberly McCall is an academic researcher from Boston University. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 32, co-authored 54 publications receiving 9070 citations. Previous affiliations of Kimberly McCall include Howard Hughes Medical Institute & Massachusetts Institute of Technology.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy 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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Searching for pattern and mutation in the Drosophila genome with a P-lacZ vector.

TL;DR: This type of screen appears to be an effective way to find new loci that may play a role in the development of the Drosophila nervous system.
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The Drosophila Gene hid Is a Direct Molecular Target of Ras-Dependent Survival Signaling

TL;DR: Evidence is presented that in Drosophila, activation of the Ras pathway specifically inhibits the proapoptotic activity of the gene head involution defective (hid), and it is shown that MAPK phosphorylation sites in Hid are critical for this response.
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Induction of apoptosis by Drosophila reaper, hid and grim through inhibition of IAP function

TL;DR: In vivo evidence is provided that the proteins encoded by reaper, hid and grim activate cell death by inhibiting the anti‐apoptotic activity of the Drosophila IAP1 (diap1) protein, providing strong in vivo evidence for a previously published model of cell death regulation in Drosophile.
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DCP-1, a Drosophila cell death protease essential for development.

TL;DR: A Drosophila caspase was identified and found to be structurally and biochemically similar to Caenorhabditis elegans CED-3, showing that this gene is essential for normal development.