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John N. Brady

Researcher at National Institutes of Health

Publications -  165
Citations -  13789

John N. Brady is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transactivation & Transcription (biology). The author has an hindex of 61, co-authored 165 publications receiving 13242 citations. Previous affiliations of John N. Brady include Instituto Politécnico Nacional.

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The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription.

TL;DR: Proteomic analysis revealed that Brd4 interacts with cyclinT1 and Cdk9 that constitutes core positive transcription elongation factor b (P-TEFb) and is a positive regulatory component of P- TEFb, which alternately interacts with Brd 4 and the inhibitory subunit to maintain functional equilibrium in the cell.
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Synergy of IL-21 and IL-15 in regulating CD8+ T cell expansion and function.

TL;DR: In vivo administration of IL-21 in combination with IL-15 boosted antigen-specific CD8+ T cell numbers and resulted in a cooperative effect on tumor regression, with apparent cures of large, established B16 melanomas.
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Characterization and isolation of stem cell–enriched human hair follicle bulge cells

TL;DR: The distribution of label-retaining cells is determined to define the human anagen bulge and CD200+ cells obtained from hair follicle suspensions demonstrated high colony-forming efficiency in clonogenic assays, indicating successful enrichment of living human bulge stem cells.
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Synergy between basic fibroblast growth factor and HIV-1 Tat protein in induction of Kaposi's sarcoma

TL;DR: Basic fibroblast growth factor and human immunodeficiency virus type 1 (HIV-1) Tat protein synergize in inducing angiogenic Kaposi's sarcoma-like lesions in mice, which may explain the higher frequency and aggressiveness of this form of KS.
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Phosphorylation of p53 serine 15 increases interaction with CBP

TL;DR: These results provide a mechanism for the activation of p53-regulated genes following DNA damage, through a signaling pathway linking p53 N-terminal kinase and C-Terminal acetyltransferase activities.