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Sally Kornbluth

Researcher at Duke University

Publications -  127
Citations -  12776

Sally Kornbluth is an academic researcher from Duke University. The author has contributed to research in topics: Apoptosis & Xenopus. The author has an hindex of 57, co-authored 127 publications receiving 12234 citations. Previous affiliations of Sally Kornbluth include University of California, San Diego & Rockefeller University.

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Reduced lipoapoptosis, hedgehog pathway activation and fibrosis in caspase-2 deficient mice with non-alcoholic steatohepatitis

TL;DR: Data point to a critical role for caspase-2 in lipid-induced hepatocyte apoptosis in vivo for the production of apoptosis-associated fibrogenic factors and in the progression of lipid- induced liver fibrosis.
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Reaper-induced dissociation of a Scythe-sequestered cytochrome c-releasing activity.

TL;DR: It is shown that Reaper binding to Scythe causes Scythe to release a sequestered apoptotic inducer, and addition of excess Scythe to egg extracts impedes Reaper‐induced apoptosis, most likely through rebinding of the released factors.
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Combinatorial control of cyclin B1 nuclear trafficking through phosphorylation at multiple sites.

TL;DR: It is reported here that phosphorylation of a single serine residue (Ser113 of Xenopus cyclin B1) abrogates nuclear export of cyclinB1 and suggests that a distinct import factor must be recruited to enhance nuclear entry of Cdc2/cyclin B 1 at the G2/M transition.
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Reaper is regulated by IAP-mediated ubiquitination

TL;DR: It is shown that the Drosophila RHG proteins (Reaper, HID, and Grim) are themselves substrates for IAP-mediated ubiquitination of Reaper, demonstrating a novel function for I APs and suggesting that IAPs and Reaper-like proteins mutually control each other's abundance.
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Differential Apaf-1 levels allow cytochrome c to induce apoptosis in brain tumors but not in normal neural tissues

TL;DR: An unexpected sensitivity of brain tumors to postmitochondrial induction of apoptosis is demonstrated and the possibility that this phenomenon could be exploited therapeutically to selectively kill brain cancer cells while sparing the surrounding brain parenchyma is raised.