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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Poliovirus-specific primer-dependent RNA polymerase able to copy poly(A).
TL;DR: Analysis of the polymerase by glycerol gradient centrifugation showed that the majority of the activity sedimented at about 4 S, indicating that it was no longer complexed with high-molecular-weight RNA or cellular membranes.
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Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines.
TL;DR: Data support the concept that heavy-chain allelic exclusion, like that of light chains, is not mediated by control at the DNA or RNA levels but is probably a consequence of feedback control from cytoplasmic mu chains.
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Separate pathways of maturation of the major structural proteins of vesicular stomatitis virus.
TL;DR: From this work it appears that the three major structural proteins come into the surface budding structure through independent pathways and together they coalesce at the plasma membrane to form the mature virion.
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Binding of Bruton's tyrosine kinase to Fyn, Lyn, or Hck through a Src homology 3 domain-mediated interaction
TL;DR: It is shown that Btk interacts with Src homology 3 domains of Fyn, Lyn, and Hck, protein-tyrosine kinases that get activated upon stimulation of B- and T-cell receptors, mediated by two 10-aa motifs in Btk.
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Role of the rasGAP-associated docking protein p62 dok in negative regulation of B cell receptor-mediated signaling
Yuji Yamanashi,Toshiki Tamura,Toshihide Kanamori,Hidehiro Yamane,Hideo Nariuchi,Tadashi Yamamoto,David Baltimore +6 more
TL;DR: It is proposed that p62(dok), a downstream target of many PTKs, plays a negative role in various signaling situations and is indispensable for FcgammaRIIB-mediated negative regulation of cell proliferation.