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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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Vectored immunoprophylaxis protects humanized mice from mucosal HIV transmission

TL;DR: It is demonstrated that VIP is capable of protecting humanized mice from intravenous as well as vaginal challenge with diverse HIV strains despite repeated exposures, suggesting that VIP may be effective in preventing vaginal transmission of HIV between humans.
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MicroRNAs, new effectors and regulators of NF-κB.

TL;DR: Since its discovery 25 years ago, nuclear factor‐κB has emerged as a transcription factor that controls diverse biological functions, ranging from inflammation to learning and memory, and both the regulation of their expression and the function of some of the non‐coding RNA genes are discussed.
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Activity of multiple light chain genes in murine myeloma cells producing a single, functional light chain

TL;DR: Two cloned lambda 1-producing myelomas (HopC-1, MOPC-104E) contain rearranged kappa genes and levels of mature-sized kappa RNA comparable to those found in kappa- producing myeloma cells, and at least two lines contain kappa protein fragments.
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Poliovirus-induced RNA polymerase and the effects of virus-specific inhibitors on its production.

TL;DR: Recent results obtained in the study of the mechanism of action of two virus- specific inhibitors are described, and evidence which bears on the virus-specific nature of theirus-induced RNA polymerase is provided.
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Regulation of NF-κB activity through lysine monomethylation of p65

TL;DR: A novel mechanism of NF-κB regulation through lysine monomethylation by SET9 methyltransferase is reported, which is required for the expression of a subset of NF -κB target genes in response to TNFα stimulation.