Memories of John N. Brady: scientist, mentor and friend.

Abstract:

:Friends and colleagues remember John N. Brady, Ph.D., Chief of the Virus Tumor Biology Section of the Laboratory of Cellular Oncology, who died much too young at the age of 57 on April 27, 2009 of colon cancer. John grew up in Illinois and received his Ph.D. with Dr. Richard Consigli at Kansas State University studying the molecular structure of polyomavirus. In 1984 John came to the National Institutes of Health as a Staff Fellow in the laboratory of Dr. Norman Salzman, Laboratory of Biology of Viruses NIAID, where he was among the first to analyze SV40 transcription using in vitro transcription systems and to analyze regulatory sequences for SV40 late transcription. He then trained with Dr. George Khoury in the Laboratory of Molecular Virology NCI, where he identified SV40 T-antigen as a transcriptional activator protein. His research interests grew to focus on the human retroviruses: human T-cell lymphotropic virus type I (HTLV-I) and human immunodeficiency virus (HIV), analyzing how interactions between these viruses and the host cell influence viral gene regulation, viral pathogenesis and viral transformation. His research also impacted the fields of eukaryotic gene regulation and tumor suppressor proteins. John is survived by his wife, Laraine, and two sons, Matt and Kevin.

journal_name

Retrovirology

journal_title

Retrovirology

authors

Pise-Masison CA,Marriott SJ

doi

10.1186/1742-4690-6-48

subject

Has Abstract

pub_date

2009-05-19 00:00:00

pages

48

issn

1742-4690

pii

1742-4690-6-48

journal_volume

6

pub_type

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  • Inhibition of Tat activity by the HEXIM1 protein.

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    pub_type: 社论,评审

    doi:10.1186/1742-4690-4-74

    authors: Yeung ML,Benkirane M,Jeang KT

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  • Human TRIM5alpha mediated restriction of different HIV-1 subtypes and Lv2 sensitive and insensitive HIV-2 variants.

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    pub_type: 杂志文章

    doi:10.1186/1742-4690-3-79

    authors: Kaumanns P,Hagmann I,Dittmar MT

    更新日期:2006-11-06 00:00:00

  • Identification of a tripartite interaction between the N-terminus of HIV-1 Vif and CBFβ that is critical for Vif function.

    abstract:BACKGROUND:HIV-1 Vif interacts with the cellular core-binding factor β (CBFβ) and counteracts the protective roles of certain human APOBEC3 (A3) proteins by targeting them for proteasomal degradation. Previous studies have identified some amino acids important for Vif-CBFβ interactions, and recently a co-crystal struct...

    journal_title:Retrovirology

    pub_type: 杂志文章

    doi:10.1186/s12977-017-0346-5

    authors: Desimmie BA,Smith JL,Matsuo H,Hu WS,Pathak VK

    更新日期:2017-03-17 00:00:00

  • Stabilization of the β-hairpin in Mason-Pfizer monkey virus capsid protein- a critical step for infectivity.

    abstract:BACKGROUND:Formation of a mature core is a crucial event for infectivity of retroviruses such as Mason-Pfizer monkey virus (M-PMV). The process is triggered by proteolytic cleavage of the polyprotein precursor Gag, which releases matrix, capsid (CA), and nucleocapsid proteins. Once released, CA assembles to form a matu...

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    pub_type: 杂志文章

    doi:10.1186/s12977-014-0094-8

    authors: Obr M,Hadravová R,DoleŽal M,KříŽová I,Papoušková V,Zídek L,Hrabal R,Ruml T,Rumlová M

    更新日期:2014-10-30 00:00:00

  • Blockade of chemokine-induced signalling inhibits CCR5-dependent HIV infection in vitro without blocking gp120/CCR5 interaction.

    abstract:BACKGROUND:Cellular infection with human immunodeficiency virus (HIV) both in vitro and in vivo requires a member of the chemokine receptor family to act as a co-receptor for viral entry. However, it is presently unclear to what extent the interaction of HIV proteins with chemokine receptors generates intracellular sig...

    journal_title:Retrovirology

    pub_type: 杂志文章

    doi:10.1186/1742-4690-2-23

    authors: Grainger DJ,Lever AM

    更新日期:2005-04-04 00:00:00