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Träfflista för sökning "WFRF:(Brodin T.) srt2:(1995-1999)"

Sökning: WFRF:(Brodin T.) > (1995-1999)

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  • Dale, S, et al. (författare)
  • A mobile tomographic gamma camera system for acute studies
  • 1997
  • Ingår i: IEEE TRANSACTIONS ON NUCLEAR SCIENCE. - : Institute of Electrical and Electronics Engineers (IEEE). - 0018-9499 .- 1558-1578. ; 44:2, s. 199-203
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Liljeholm, S, et al. (författare)
  • NF-kappaB only partially mediates Epstein-Barr virus latent membrane protein 1 activation of B cells.
  • 1998
  • Ingår i: Journal of General Virology. - 0022-1317 .- 1465-2099. ; 79 ( Pt 9), s. 2117-25
  • Tidskriftsartikel (refereegranskat)abstract
    • The latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) is required for EBV-induced immortalization of human B cells and causes tumorigenic transformation of cell lines. LMP1 expression induces phenotypic changes resembling B cell activation, such as cell size increase and up-regulation of cell surface activation markers. LMP1 contains two domains that activate the transcription factor NF-kappaB, one through interactions with TRAF proteins and the other with the TRADD protein. The purpose of the present study was to investigate the importance of NF-kappaB induction in the up-regulation of the B cell activation markers ICAM-1 and CD71 by LMP1. This study shows that expression of LMP1 activates transcription from p50/p65- and c-Rel-responsive promoters, and that this activity can be completely inhibited by expression of a dominant inhibitory IkappaB mutant. ICAM-1 and CD71 are nevertheless up-regulated by LMP1 in primary B cells and cell lines expressing the dominant IkappaB. Furthermore, LMP1-induced cell size increase of primary B cells was unaffected by IkappaB expression. It was concluded that even when LMP1 is unable to activate NF-kappaB, it is still capable of inducing certain characteristics of activated B cells, strongly suggesting that LMP1 can also activate cells independently of NF-kappaB.
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