D
David Baltimore
Researcher at California Institute of Technology
Publications - 882
Citations - 168784
David Baltimore is an academic researcher from California Institute of Technology. The author has contributed to research in topics: RNA & Virus. The author has an hindex of 203, co-authored 876 publications receiving 162955 citations. Previous affiliations of David Baltimore include Thomas Jefferson University & Johns Hopkins University.
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Journal ArticleDOI
IκBβ acts to inhibit and activate gene expression during the inflammatory response
Ping Rao,Matthew S. Hayden,Matthew S. Hayden,Meixiao Long,Meixiao Long,Martin L. Scott,Martin L. Scott,A. Philip West,Dekai Zhang,Dekai Zhang,Andrea Oeckinghaus,Andrea Oeckinghaus,Candace Lynch,Alexander Hoffmann,David Baltimore,Sankar Ghosh,Sankar Ghosh +16 more
TL;DR: In vivo IκBβ serves both to inhibit and facilitate the inflammatory response, and might be a promising new strategy for selectively inhibiting the chronic phase of TNF-α production during theinflammatory response.
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Epistasis between MicroRNAs 155 and 146a during T Cell-Mediated Antitumor Immunity
Thomas B. Huffaker,Ruozhen Hu,Marah C. Runtsch,Erin Bake,Xinjian Chen,Jimmy L. Zhao,June L. Round,David Baltimore,Ryan M. O'Connell +8 more
TL;DR: This work reveals critical roles for miRNAs in the reciprocal regulation of CD4(+) and CD8(+) T cell-mediated antitumor immunity and demonstrates the dominant nature of miR-155 during its promotion of immune responses.
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Stable reduction of CCR5 by RNAi through hematopoietic stem cell transplant in non-human primates.
Dong Sung An,Robert E. Donahue,Masakazu Kamata,Betty Poon,Mark E. Metzger,Si-Hua Mao,Aylin C. Bonifacino,Allen E. Krouse,Jean-Luc Darlix,David Baltimore,F. Xiao-Feng Qin,Irvin S. Y. Chen +11 more
TL;DR: These studies provide a successful demonstration that siRNAs can be used together with hematopoietic stem cell transplant to stably modulate gene expression in primates and potentially treat blood diseases such as HIV-1.
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The gene for enhancer binding proteins E12/E47 lies at the t(1;19) breakpoint in acute leukemias.
Julia D. Mellentin,Cornelis Murre,Timothy A. Donlon,Patrick S. McCaw,Stephen D. Smith,Andrew J. Carroll,Marcy E. McDonald,David Baltimore,Michael L. Cleary +8 more
TL;DR: Observations indicate that the gene for a transcription factor is located at the breakpoint of a consistently recurring chromosomal translocation in many acute leukemias and suggest a direct role for alteration of such factors in the pathogenesis of some malignancies.
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B-cell- and myocyte-specific E2-box-binding factors contain E12/E47-like subunits.
TL;DR: It is demonstrated here that E2-box-binding B-cell- and myocyte-specific nuclear factors contain subunits which are identical or closely related to ubiquitously expressed (E12/E47) HLH proteins, similar to the genetically defined function of daughterless in Drosophila development.