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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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HIV-1 Nef protein protects infected primary cells against killing by cytotoxic T lymphocytes

TL;DR: It is found that CTLs inefficiently lysed primary cells infected with HIV-1 if the viral nef gene product was expressed and Nef protected infected cells by reducing the epitope density on their surface.
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Modular binding domains in signal transduction proteins

TL;DR: The transduction of a signal is a change in form of the signal as it is passed from one carrier to another, and the signal transduction protein must be highly integrated, with all of the elements working together to send just the appropriate quanta of signal for the specific need.
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ATR disruption leads to chromosomal fragmentation and early embryonic lethality.

TL;DR: Data show that ATR is essential for early embryonic development and must function in processes other than regulation of p53, implying that apoptosis is caused by a loss of genomic integrity.
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A nuclear factor that binds to a conserved sequence motif in transcriptional control elements of immunoglobulin genes.

TL;DR: It is reported here the identification of a human B-cell nuclear factor (IgNF-A) that binds to DNA sequences in the upstream regions of both the mouse heavy and κ light-chain gene promoters and also to the mouseHeavychain gene enhancer.
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The selective downregulation of class I major histocompatibility complex proteins by HIV-1 protects HIV-infected cells from NK cells.

TL;DR: Subpopulations of CTL and NK cells may be uniquely suited for combating HIV, and evidence that HIV-1 selectively downregulates HLA-A andHLA-B but does not significantly affect H LA-C or HLAE is presented.