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Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick

Currently, there is a paucity of information regarding the molecular pathogenesis for many high‐consequence pathogens (HCPs) that pose threats to both national and international public health. In spite of this, investigations of the molecular pathogenesis for many HCPs have been limited to gross pat...

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Detalles Bibliográficos
Autores principales: Kindrachuk, Jason, Falcinelli, Shane, Wada, Jiro, Kuhn, Jens H., Hensley, Lisa E., Jahrling, Peter B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6136422/
https://www.ncbi.nlm.nih.gov/pubmed/24585711
http://dx.doi.org/10.1111/2049-632X.12163
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author Kindrachuk, Jason
Falcinelli, Shane
Wada, Jiro
Kuhn, Jens H.
Hensley, Lisa E.
Jahrling, Peter B.
author_facet Kindrachuk, Jason
Falcinelli, Shane
Wada, Jiro
Kuhn, Jens H.
Hensley, Lisa E.
Jahrling, Peter B.
author_sort Kindrachuk, Jason
collection PubMed
description Currently, there is a paucity of information regarding the molecular pathogenesis for many high‐consequence pathogens (HCPs) that pose threats to both national and international public health. In spite of this, investigations of the molecular pathogenesis for many HCPs have been limited to gross pathological changes in animal models or global analysis of gene expression. Further, questions remain regarding the ability of animal models of disease to recapitulate human molecular pathogenesis or act as predictors of therapeutic efficacy. Thus, it is likely that medical countermeasure development for HCPs will rely on identifying therapeutic targets that are uniquely modulated during HCP infection. It is also appreciated that many cellular processes can be regulated independently of changes in transcription or translation through phosphorylation events. Cellular kinases, individually or collectively (the kinome), play critical roles in regulating complex biology, underlie various malignancies, and represent high‐priority drug targets. The growing interest in kinases in both basic and translational research has driven efforts to develop technologies that enable characterization of phosphorylation‐mediated signal transduction. To this end, enhanced technical capabilities at the IRF‐Frederick provide the unique capability for characterizing host responses to HCP insult during the course of infection and identify novel targets for therapeutic intervention.
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spelling pubmed-61364222018-09-13 Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick Kindrachuk, Jason Falcinelli, Shane Wada, Jiro Kuhn, Jens H. Hensley, Lisa E. Jahrling, Peter B. Pathog Dis MiniReviews Currently, there is a paucity of information regarding the molecular pathogenesis for many high‐consequence pathogens (HCPs) that pose threats to both national and international public health. In spite of this, investigations of the molecular pathogenesis for many HCPs have been limited to gross pathological changes in animal models or global analysis of gene expression. Further, questions remain regarding the ability of animal models of disease to recapitulate human molecular pathogenesis or act as predictors of therapeutic efficacy. Thus, it is likely that medical countermeasure development for HCPs will rely on identifying therapeutic targets that are uniquely modulated during HCP infection. It is also appreciated that many cellular processes can be regulated independently of changes in transcription or translation through phosphorylation events. Cellular kinases, individually or collectively (the kinome), play critical roles in regulating complex biology, underlie various malignancies, and represent high‐priority drug targets. The growing interest in kinases in both basic and translational research has driven efforts to develop technologies that enable characterization of phosphorylation‐mediated signal transduction. To this end, enhanced technical capabilities at the IRF‐Frederick provide the unique capability for characterizing host responses to HCP insult during the course of infection and identify novel targets for therapeutic intervention. John Wiley and Sons Inc. 2014-07 2014-04-10 /pmc/articles/PMC6136422/ /pubmed/24585711 http://dx.doi.org/10.1111/2049-632X.12163 Text en Published 2014. This article is a US Government work and is in the public domain in the USA. This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.
spellingShingle MiniReviews
Kindrachuk, Jason
Falcinelli, Shane
Wada, Jiro
Kuhn, Jens H.
Hensley, Lisa E.
Jahrling, Peter B.
Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title_full Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title_fullStr Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title_full_unstemmed Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title_short Systems kinomics for characterizing host responses to high‐consequence pathogens at the NIH/NIAID Integrated Research Facility‐Frederick
title_sort systems kinomics for characterizing host responses to high‐consequence pathogens at the nih/niaid integrated research facility‐frederick
topic MiniReviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6136422/
https://www.ncbi.nlm.nih.gov/pubmed/24585711
http://dx.doi.org/10.1111/2049-632X.12163
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