Identification of cellular target genes of the Epstein-Barr virus transactivator Zta: activation of transforming growth factor beta igh3 (TGF-beta igh3) and TGF-beta 1 (Q35841284)

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scientific article published in July 1995

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English	Identification of cellular target genes of the Epstein-Barr virus transactivator Zta: activation of transforming growth factor beta igh3 (TGF-beta igh3) and TGF-beta 1	scientific article published in July 1995

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scholarly article

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25 October 2019

Identification of cellular target genes of the Epstein-Barr virus transactivator Zta: activation of transforming growth factor beta igh3 (TGF-beta igh3) and TGF-beta 1 (English)

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25 October 2019

Epstein–Barr virus

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author name string

C Cayrol

1

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25 October 2019

E K Flemington

2

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publication date

1 July 1995

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25 October 2019

Journal of Virology

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25 October 2019

69

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7

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25 October 2019

4206-4212

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25 October 2019

The ZEBRA activation domain: modular organization and mechanism of action

1 reference

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Only the HLA class I gene minimal promoter elements are required for transactivation by human cytomegalovirus immediate early genes.

1 reference

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Epstein-Barr virus-induced genes: first lymphocyte-specific G protein-coupled peptide receptors

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DNA-binding-defective mutants of the Epstein-Barr virus lytic switch activator Zta transactivate with altered specificities

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Modulation of major histocompatibility complex antigen expression by viral infection

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Human cytomegalovirus infection induces transcription and secretion of transforming growth factor beta 1

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beta ig-h3: a transforming growth factor-beta-responsive gene encoding a secreted protein that inhibits cell attachment in vitro and suppresses the growth of CHO cells in nude mice

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DNA sequence and expression of the B95-8 Epstein-Barr virus genome.

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Activated lymphocytes during acute Epstein-Barr virus infection

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Transfection of a rearranged viral DNA fragment, WZhet, stably converts latent Epstein-Barr viral infection to productive infection in lymphoid cells.

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A second site for Epstein-Barr virus shedding: the uterine cervix

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Polymorphic proteins encoded within BZLF1 of defective and standard Epstein-Barr viruses disrupt latency

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Activation of the second promoter of the transforming growth factor-beta 1 gene by transforming growth factor-beta 1 and phorbol ester occurs through the same target sequences.

1 reference

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Transforming growth factor beta specifically enhances IgA production by lipopolysaccharide-stimulated murine B lymphocytes

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The Epstein-Barr virus early protein EB1 activates transcription from different responsive elements including AP-1 binding sites

1 reference

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The Epstein-Barr virus BMLF1 promoter contains an enhancer element that is responsive to the BZLF1 and BRLF1 transactivators

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Epstein-Barr virus BZLF1 trans-activator specifically binds to a consensus AP-1 site and is related to c-fos

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An intricate route to immortality

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Transactivation of the transforming growth factor beta 1 (TGF-beta 1) gene by human T lymphotropic virus type 1 tax: a potential mechanism for the increased production of TGF-beta 1 in adult T cell leukemia

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Evidence for coiled-coil dimer formation by an Epstein-Barr virus transactivator that lacks a heptad repeat of leucine residues

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Epstein-Barr virus BZLF1 trans activator induces the promoter of a cellular cognate gene, c-fos

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The Epstein-Barr virus Zta transactivator: a member of the bZIP family with unique DNA-binding specificity and a dimerization domain that lacks the characteristic heptad leucine zipper motif.

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In vitro transcriptional activation, dimerization, and DNA-binding specificity of the Epstein-Barr virus Zta protein

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Structure and function of the Epstein-Barr virus BZLF1 protein

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Autoregulation of Epstein-Barr virus putative lytic switch gene BZLF1.

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The zta transactivator involved in induction of lytic cycle gene expression in Epstein-Barr virus-infected lymphocytes binds to both AP-1 and ZRE sites in target promoter and enhancer regions.

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Autoinduction of transforming growth factor beta 1 is mediated by the AP-1 complex

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Identifiers

10.1128/JVI.69.7.4206-4212.1995

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1 reference

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25 October 2019

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Europe PubMed Central

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25 October 2019

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