Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Gillian A, Parker"'
Autor:
Christine T Styles, Quentin Bazot, Gillian A Parker, Robert E White, Kostas Paschos, Martin J Allday
Publikováno v:
PLoS Biology, Vol 15, Iss 8, p e2001992 (2017)
Mature human B cells infected by Epstein-Barr virus (EBV) become activated, grow, and proliferate. If the cells are infected ex vivo, they are transformed into continuously proliferating lymphoblastoid cell lines (LCLs) that carry EBV DNA as extra-ch
Externí odkaz:
https://doaj.org/article/5d007c99841c4a07b1e2e58730427abe
Autor:
Quentin Bazot, Kostas Paschos, Lenka Skalska, Jens S Kalchschmidt, Gillian A Parker, Martin J Allday
Publikováno v:
PLoS Pathogens, Vol 11, Iss 7, p e1005031 (2015)
We show that two host-encoded primary RNAs (pri-miRs) and the corresponding microRNA (miR) clusters--widely reported to have cell transformation-associated activity--are regulated by EBNA3A and EBNA3C. Utilising a variety of EBV-transformed lymphobla
Externí odkaz:
https://doaj.org/article/5df2e90ec487485f89827bb3463b05d7
Autor:
Lenka Skalska, Robert E. White, Gillian A. Parker, Ernest Turro, Alison J. Sinclair, Kostas Paschos, Martin J. Allday
Publikováno v:
PLoS Pathogens, Vol 9, Iss 3 (2013)
Externí odkaz:
https://doaj.org/article/25147c91da714e85910512111daf0f46
Autor:
Lenka Skalska, Robert E White, Gillian A Parker, Ernest Turro, Alison J Sinclair, Kostas Paschos, Martin J Allday
Publikováno v:
PLoS Pathogens, Vol 9, Iss 2, p e1003187 (2013)
To explore the role of p16(INK4a) as an intrinsic barrier to B cell transformation by EBV, we transformed primary B cells from an individual homozygous for a deletion in the CDKN2A locus encoding p16(INK4a) and p14(ARF). Using recombinant EBV-BAC vir
Externí odkaz:
https://doaj.org/article/28b56d54882a42acada95ed3eb0c789a
Autor:
Christine T. Styles, Kostas Paschos, Gillian A. Parker, Martin J. Allday, Quentin Bazot, Robert E. White
Publikováno v:
PLoS Biology
PLoS Biology, Vol 15, Iss 8, p e2001992 (2017)
PLoS Biology, Vol 15, Iss 8, p e2001992 (2017)
Mature human B cells infected by Epstein-Barr virus (EBV) become activated, grow, and proliferate. If the cells are infected ex vivo, they are transformed into continuously proliferating lymphoblastoid cell lines (LCLs) that carry EBV DNA as extra-ch
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c005f0f5215631b0419423a48884c64
http://hdl.handle.net/10044/1/52043
http://hdl.handle.net/10044/1/52043
Autor:
Kostas, Paschos, Quentin, Bazot, Guiyi, Ho, Gillian A, Parker, Jonathan, Lees, Geraint, Barton, Martin J, Allday
Publikováno v:
Nucleic Acids Research
ChIP-seq performed on lymphoblastoid cell lines (LCLs), expressing epitope-tagged EBNA3A, EBNA3B or EBNA3C from EBV-recombinants, revealed important principles of EBNA3 binding to chromatin. When combined with global chromatin looping data, EBNA3-bou
Publikováno v:
Nucleic Acids Research
Detailed analyses of the chromatin around the BIM promoter has revealed that latent Epstein–Barr virus (EBV) triggers the recruitment of polycomb repressive complex 2 (PRC2) core subunits and the trimethylation of histone H3 lysine 27 (H3K27me3) at
Publikováno v:
Journal of Virology. 75:2400-2410
Expression of the lytic cycle genes of Epstain-Barr virus (EBV) is induced in type I Burkitt's lymphoma-derived cells by treatment with phorbol esters (e.g., phorbol myristate acetate [PMA]), anti-immunoglobulin, or the cytokine transforming growth f
Autor:
Pinchas Osin, Martin J. Allday, Louise Brooks, Susan Crossland, Karen Barker, Paul D. Smith, Elizabeth Philp, Tim Crook, Joanne Waller, Isik G. Yulug, Barry A. Gusterson, Julian Peto, Mark R. Crompton, Gillian A. Parker
Publikováno v:
Oncogene. 17:1681-1689
The status of p53 was investigated in breast tumours arising in germ-line carriers of mutant alleles of BRCA1 and BRCA2 and in a control series of sporadic breast tumours. p53 expression was detected in 20/26 (77%) BRCA1-, 10/22 (45%) BRCA2-associate
Autor:
Lenka, Skalska, Robert E, White, Gillian A, Parker, Ernest, Turro, Alison J, Sinclair, Kostas, Paschos, Martin J, Allday
Publikováno v:
PLoS Pathogens
PLoS Pathogens, Vol 9, Iss 2, p e1003187 (2013)
PLoS Pathogens, Vol 9, Iss 2, p e1003187 (2013)
To explore the role of p16INK4a as an intrinsic barrier to B cell transformation by EBV, we transformed primary B cells from an individual homozygous for a deletion in the CDKN2A locus encoding p16INK4a and p14ARF. Using recombinant EBV-BAC viruses e