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Hisashi Harada

Researcher at Virginia Commonwealth University

Publications -  114
Citations -  21125

Hisashi Harada is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 47, co-authored 112 publications receiving 19531 citations. Previous affiliations of Hisashi Harada include Washington University in St. Louis & University of New Mexico.

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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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Serine Phosphorylation of Death Agonist BAD in Response to Survival Factor Results in Binding to 14-3-3 Not BCL-XL

TL;DR: The rapid phosphorylation of BAD following IL-3 connects a proximal survival signal with the BCL-2 family, modulating this checkpoint for apoptosis and enhanced BAD's death-promoting activity.
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Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin

TL;DR: The molecular cloning, structural analysis and functional expression of the cDNA encoding human B SF-2 indicated that BSF-2 is functionally and structurally unlike other known proteins.
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Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-β gene regulatory elements

TL;DR: It is shown here that the IRF-1 gene possesses virus-inducible promoter and is also involved in the regulation of other genes such as IFN-alpha and MHC class I genes.
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Structurally similar but functionally distinct factors, IRF-1 and IRF-2, bind to the same regulatory elements of IFN and IFN-inducible genes

TL;DR: The results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.