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Hermann Steller

Researcher at Rockefeller University

Publications -  121
Citations -  21474

Hermann Steller is an academic researcher from Rockefeller University. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 64, co-authored 120 publications receiving 20320 citations. Previous affiliations of Hermann Steller include University of California, Berkeley & Massachusetts Institute of Technology.

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Mechanisms and genes of cellular suicide

TL;DR: Genetic studies in the nematode Caenorhabditis elegans and in the fruit fly Drosophila melanogaster have led to the isolation of genes that are specifically required for the induction of programmed cell death.
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Lorenzo Galluzzi, +103 more
TL;DR: A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
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Programmed Cell Death in Animal Development and Disease

TL;DR: A growing body of work about the connections between apoptosis, stem cells, and cancer is explored, focusing on how apoptotic cells release a variety of signals to communicate with their cellular environment, including factors that promote cell division, tissue regeneration, and wound healing.
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Genetic control of programmed cell death in Drosophila

TL;DR: A gene, reaper (rpr), that appears to play a central control function for the initiation of programmed cell death (apoptosis) in Drosophila was identified and suggests that the basic cell death program is intact although it was not activated in mutant embryos.
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The head involution defective gene of Drosophila melanogaster functions in programmed cell death.

TL;DR: The hid gene appears to encode a novel 410-amino-acid protein, and its mRNA is expressed in regions of the embryo where cell death occurs, and can be suppressed completely by expression of the anti-apoptotic p35 protein from baculovirus.