Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophages
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Immunity around the clock.Disease tolerance and immunity in host protection against infection.Thrombospondin1 (TSP1) replacement prevents cerebral cavernous malformations.Pharmacological inhibition of REV-ERB stimulates differentiation, inhibits turnover and reduces fibrosis in dystrophic muscle.Transcriptional repression in macrophages-basic mechanisms and alterations in metabolic inflammatory diseases.Circadian clock component REV-ERBα controls homeostatic regulation of pulmonary inflammation.Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failureRequirement for NF-κB in maintenance of molecular and behavioral circadian rhythms in miceDamage-associated molecular patterns in inflammatory bowel disease: From biomarkers to therapeutic targets
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Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophages
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 27 July 2016
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Tissue damage drives co-locali ...... nd repair in mouse macrophages
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Tissue damage drives co-locali ...... d repair in mouse macrophages.
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type
label
Tissue damage drives co-locali ...... nd repair in mouse macrophages
@en
Tissue damage drives co-locali ...... d repair in mouse macrophages.
@nl
prefLabel
Tissue damage drives co-locali ...... nd repair in mouse macrophages
@en
Tissue damage drives co-locali ...... d repair in mouse macrophages.
@nl
P2093
P2860
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Tissue damage drives co-locali ...... nd repair in mouse macrophages
@en
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David Gosselin
Hanna P Lesch
Jenhan Tao
Michael T Lam
Nathanael J Spann
Richard L Gallo
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P356
10.7554/ELIFE.13024
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P577
2016-07-27T00:00:00Z