Lista de obras - Robert E White - Dominio Público Uruguay

An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells

artículo científico publicado en 2010

BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV

artículo científico publicado en 2012

Cellular gene expression that correlates with EBER expression in Epstein-Barr Virus-infected lymphoblastoid cell lines

artículo científico publicado en 2011

Correction: Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome

artículo científico publicado en 2019

Correction: Induction of p16INK4a Is the Major Barrier to Proliferation when Epstein-Barr Virus (EBV) Transforms Primary B Cells into Lymphoblastoid Cell Lines.

artículo científico publicado en 2013

Development of herpesvirus-based episomally maintained gene delivery vectors

artículo científico publicado en 2004

EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors

artículo científico publicado en 2012

EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency

artículo científico publicado en 2017

Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.

artículo científico publicado en 2010

Epstein-Barr virus nuclear antigen (EBNA) 3A induces the expression of and interacts with a subset of chaperones and co-chaperones.

artículo científico publicado en 2008

Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome.

artículo científico publicado en 2018

Epstein-Barr virus origin of lytic replication mediates association of replicating episomes with promyelocytic leukaemia protein nuclear bodies and replication compartments

artículo científico publicado en 2006

Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim

artículo científico publicado en 2009

Essential role of inverted repeat in Epstein-Barr virus IR-1 in B cell transformation; geographical variation of the viral genome

artículo científico publicado en 2019

Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification

artículo científico publicado en 2010

Functional delivery of large genomic DNA to human cells with a peptide-lipid vector

artículo científico publicado en 2003

Generation and precise modification of a herpesvirus saimiri bacterial artificial chromosome demonstrates that the terminal repeats are required for both virus production and episomal persistence

artículo científico publicado en 2003

Genome diversity of Epstein-Barr virus from multiple tumor types and normal infection

artículo científico publicado en 2015

Heterogeneity of the Epstein-Barr virus major internal repeat reveals evolutionary mechanisms of EBV and a functional defect in the prototype EBV strain B95-8.

artículo científico publicado en 2017

Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines

artículo científico publicado en 2013

Infectious delivery of 120-kilobase genomic DNA by an epstein-barr virus amplicon vector

artículo científico publicado en 2002

Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expression

artículo científico publicado en 2011

Mutagenesis of the herpesvirus saimiri terminal repeat region reveals important elements for virus production

artículo científico publicado en 2007

Natural Variation of Epstein-Barr Virus Genes, Proteins, and Primary MicroRNA.

artículo científico publicado en 2017

Open reading frame 73 is required for herpesvirus saimiri A11-S4 episomal persistence

artículo científico publicado en 2005

Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression.

artículo científico

Production of an infectious Herpesvirus saimiri-based episomally maintained amplicon system

artículo científico publicado en 2008

Sequence Variation of Epstein-Barr Virus: Viral Types, Geography, Codon Usage, and Diseases

artículo científico publicado en 2018

The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.

artículo científico publicado en 2018

The EBNA3 Family: Two Oncoproteins and a Tumour Suppressor that Are Central to the Biology of EBV in B Cells

artículo científico

Two Epstein-Barr virus (EBV) oncoproteins cooperate to repress expression of the proapoptotic tumour-suppressor Bim: clues to the pathogenesis of Burkitt's lymphoma.

artículo científico publicado en 2007

Lista de obras de Robert E White

An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells

BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV

Cellular gene expression that correlates with EBER expression in Epstein-Barr Virus-infected lymphoblastoid cell lines

Correction: Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome

Correction: Induction of p16INK4a Is the Major Barrier to Proliferation when Epstein-Barr Virus (EBV) Transforms Primary B Cells into Lymphoblastoid Cell Lines.

Development of herpesvirus-based episomally maintained gene delivery vectors

EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors

EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency

Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.

Epstein-Barr virus nuclear antigen (EBNA) 3A induces the expression of and interacts with a subset of chaperones and co-chaperones.

Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome.

Epstein-Barr virus origin of lytic replication mediates association of replicating episomes with promyelocytic leukaemia protein nuclear bodies and replication compartments

Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim

Essential role of inverted repeat in Epstein-Barr virus IR-1 in B cell transformation; geographical variation of the viral genome

Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification

Functional delivery of large genomic DNA to human cells with a peptide-lipid vector

Generation and precise modification of a herpesvirus saimiri bacterial artificial chromosome demonstrates that the terminal repeats are required for both virus production and episomal persistence

Genome diversity of Epstein-Barr virus from multiple tumor types and normal infection

Heterogeneity of the Epstein-Barr virus major internal repeat reveals evolutionary mechanisms of EBV and a functional defect in the prototype EBV strain B95-8.

Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines

Infectious delivery of 120-kilobase genomic DNA by an epstein-barr virus amplicon vector

Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expression

Mutagenesis of the herpesvirus saimiri terminal repeat region reveals important elements for virus production

Natural Variation of Epstein-Barr Virus Genes, Proteins, and Primary MicroRNA.

Open reading frame 73 is required for herpesvirus saimiri A11-S4 episomal persistence

Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression.

Production of an infectious Herpesvirus saimiri-based episomally maintained amplicon system

Sequence Variation of Epstein-Barr Virus: Viral Types, Geography, Codon Usage, and Diseases

The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.

The EBNA3 Family: Two Oncoproteins and a Tumour Suppressor that Are Central to the Biology of EBV in B Cells

Two Epstein-Barr virus (EBV) oncoproteins cooperate to repress expression of the proapoptotic tumour-suppressor Bim: clues to the pathogenesis of Burkitt's lymphoma.