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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Targeted disruption of ATM leads to growth retardation, chromosomal fragmentation during meiosis, immune defects, and thymic lymphoma.
TL;DR: Findings indicate that the ATM gene product plays an essential role in a diverse group of cellular processes, including meiosis, the normal growth of somatic tissues, immune development, and tumor suppression.
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Function of miR-146a in Controlling Treg Cell-Mediated Regulation of Th1 Responses
Li-Fan Lu,Mark Boldin,Ashutosh Chaudhry,Ling Li Lin,Konstantin Taganov,Toshikatsu Hanada,Akihiko Yoshimura,David Baltimore,David Baltimore,Alexander Y. Rudensky +9 more
TL;DR: It is reported that miR-146a, one of the miRNAs prevalently expressed in Treg cells, is critical for their suppressor function and that an optimal range of Stat1 activation is important for Treg-mediated control of Th1 responses and associated autoimmunity.
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Functional activity of myogenic HLH proteins requires hetero-oligomerization with E12/E47-like proteins in vivo
Andrew B. Lassar,Robert L. Davis,Woodring E. Wright,Tom Kadesch,Cornelis Murre,Anna Voronova,David Baltimore,Harold Weintraub +7 more
TL;DR: It is demonstrated that MyoD, in conjunction with E12/E47-like proteins, is functioning as a regulatory nodal point for activation of several other downstream muscle regulators.
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The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene.
TL;DR: By analogy to the gag/abl fusion protein of Abelson murine leukemia virus, the replacement of amino terminal c-abl sequences by bcr sequences in P210 may create a transforming protein involved in CML.
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MicroRNA-155 Promotes Autoimmune Inflammation by Enhancing Inflammatory T Cell Development
Ryan M. O'Connell,Daniel Kahn,Daniel Kahn,William S. Gibson,June L. Round,Rebecca L. Scholz,Aadel A. Chaudhuri,Melissa Kahn,Dinesh S. Rao,Dinesh S. Rao,David Baltimore +10 more
TL;DR: It is shown that one aspect of miR-155 function is the promotion of T cell-dependent tissue inflammation, suggesting that miR -155 might be a promising therapeutic target for the treatment of autoimmune disorders.