Severe acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling (Q28259664)

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English	Severe acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling	scientific article

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scholarly article

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Severe acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling (English)

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viral nucleocapsid

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based on heuristic

inferred from title

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nucleoprotein [SARS-Cov]

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1 reference

based on heuristic

inferred from title

author name string

Xingang Zhao

1

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John M Nicholls

2

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Ye-Guang Chen

3

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language of work or name

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publication date

8 February 2008

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Journal of Biological Chemistry

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283

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6

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3272-80

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The Genome sequence of the SARS-associated coronavirus

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Characterization of a novel coronavirus associated with severe acute respiratory syndrome

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Assembly of severe acute respiratory syndrome coronavirus RNA packaging signal into virus-like particles is nucleocapsid dependent

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Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists

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The SARS coronavirus nucleocapsid protein induces actin reorganization and apoptosis in COS-1 cells in the absence of growth factors

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The nucleocapsid protein of severe acute respiratory syndrome-coronavirus inhibits the activity of cyclin-cyclin-dependent kinase complex and blocks S phase progression in mammalian cells

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Cytostatic and apoptotic actions of TGF-beta in homeostasis and cancer

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Smad3 is key to TGF-beta-mediated epithelial-to-mesenchymal transition, fibrosis, tumor suppression and metastasis.

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Transforming growth factor beta in tissue fibrosis

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Mechanisms of TGF-beta signaling from cell membrane to the nucleus

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Smad transcription factors

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Specificity and versatility in tgf-beta signaling through Smads

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The clinical pathology of severe acute respiratory syndrome (SARS): a report from China

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Lung pathology of fatal severe acute respiratory syndrome.

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Time course and cellular localization of SARS-CoV nucleoprotein and RNA in lungs from fatal cases of SARS.

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Inhibition of severe acute respiratory syndrome virus replication by small interfering RNAs in mammalian cells

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Dapper 1 antagonizes Wnt signaling by promoting dishevelled degradation

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PPM1A functions as a Smad phosphatase to terminate TGFbeta signaling

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Smad7 antagonizes transforming growth factor beta signaling in the nucleus by interfering with functional Smad-DNA complex formation

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Direct binding of Smad3 and Smad4 to critical TGF beta-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene

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Type I receptors specify growth-inhibitory and transcriptional responses to transforming growth factor beta and activin

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Smad4 and FAST-1 in the assembly of activin-responsive factor

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OAZ uses distinct DNA- and protein-binding zinc fingers in separate BMP-Smad and Olf signaling pathways

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Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis

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Amino acid residues critical for RNA-binding in the N-terminal domain of the nucleocapsid protein are essential determinants for the infectivity of coronavirus in cultured cells

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The nucleocapsid protein of the SARS coronavirus is capable of self-association through a C-terminal 209 amino acid interaction domain

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Intracellular localization of the severe acute respiratory syndrome coronavirus nucleocapsid protein: absence of nucleolar accumulation during infection and after expression as a recombinant protein in vero cells

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Nuclear/nucleolar localization properties of C-terminal nucleocapsid protein of SARS coronavirus

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TGF-beta-stimulated cooperation of smad proteins with the coactivators CBP/p300

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M708033200

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The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for smad3 in TGF-beta-induced transcriptional activation

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TGF-beta-induced phosphorylation of Smad3 regulates its interaction with coactivator p300/CREB-binding protein

1 reference

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Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.

1 reference

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Induction of apoptosis by Smad3 and down-regulation of Smad3 expression in response to TGF-beta in human normal lung epithelial cells

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Nucleocapsid protein as early diagnostic marker for SARS.

1 reference

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Hepatitis C viral proteins interact with Smad3 and differentially regulate TGF-beta/Smad3-mediated transcriptional activation

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Modulation of the transforming growth factor-beta signal transduction pathway by hepatitis C virus nonstructural 5A protein

1 reference

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The hepatitis B virus encoded oncoprotein pX amplifies TGF-beta family signaling through direct interaction with Smad4: potential mechanism of hepatitis B virus-induced liver fibrosis

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Human T-cell lymphotropic virus type 1 tax inhibits transforming growth factor-beta signaling by blocking the association of Smad proteins with Smad-binding element

1 reference

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Inhibition of transforming growth factor beta signaling and Smad-dependent activation of transcription by the Latent Membrane Protein 1 of Epstein-Barr virus

1 reference

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Bleomycin-induced pulmonary fibrosis in transgenic mice that either lack or overexpress the murine plasminogen activator inhibitor-1 gene

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Regulation of plasminogen activator inhibitor-1 expression by transforming growth factor-beta -induced physical and functional interactions between smads and Sp1.

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Synergistic cooperation of TFE3 and smad proteins in TGF-beta-induced transcription of the plasminogen activator inhibitor-1 gene

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Targeted disruption in murine cells reveals variable requirement for Smad4 in transforming growth factor beta-related signaling.

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Hematopoiesis controlled by distinct TIF1gamma and Smad4 branches of the TGFbeta pathway

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Overexpression of 7a, a protein specifically encoded by the severe acute respiratory syndrome coronavirus, induces apoptosis via a caspase-dependent pathway

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G0/G1 arrest and apoptosis induced by SARS-CoV 3b protein in transfected cells

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The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells.

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Viruses and Apoptosis

1 reference

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Identifiers

10.1074/JBC.M708033200

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

OpenCitations bibliographic resource ID

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

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