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Scott H. Kaufmann
Researcher at Mayo Clinic
Publications - 485
Citations - 48694
Scott H. Kaufmann is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Apoptosis & Ovarian cancer. The author has an hindex of 105, co-authored 464 publications receiving 45654 citations. Previous affiliations of Scott H. Kaufmann include Johns Hopkins University School of Medicine & Karolinska Institutet.
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Mammalian caspases: structure ,a ctivation ,s ubstrates, and functions during apoptosis
TL;DR: Caspases, a family of cysteine-dependent aspartate-directed proteases, are prominent among the death proteases as discussed by the authors, and they play critical roles in initiation and execution of this process.
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Mammalian Caspases: Structure, Activation, Substrates, and Functions During Apoptosis
TL;DR: This work has shown that apoptotic cell death is a genetically programmed, morphologically distinct form of cell death that can be triggered by a variety of physiological and pathological stimuli, and that proteases play critical roles in initiation and execution of this process.
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Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE
TL;DR: A novel protease resembling ICE (prICE) that is active in a cell-free system that reproduces the morphological and biochemical events of apoptosis in the extracts including morphological changes, cleavage of PARP and production of an oligonucleosomal ladder.
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Specific Proteolytic Cleavage of Poly(ADP-ribose) Polymerase: An Early Marker of Chemotherapy-induced Apoptosis
TL;DR: The results suggest that proteolytic cleavage of pADPRp, in addition to being an early marker of chemotherapy-induced apoptosis, might reflect more widespread proteolysis that is a critical biochemical event early during the process of physiological cell death.
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Induction of apoptosis by cancer chemotherapy.
TL;DR: The two prototypic death pathways are described, current understanding of the role of the two pathways in chemotherapy-induced apoptosis is summarized, and the implications of these studies for mechanisms of resistance to chemotherapeutic agents are discussed.