%D8%A5%D9%8A%D9%81%D8%A7_%D9%83%D9%84%D8%A7%D9%8A%D9%86%D0%95%D0%B2%D0%B0_%D0%9A%D0%BB%D1%8F%D0%B9%D0%BDEva_Klein%CE%95%CF%8D%CE%B1_%CE%9A%CE%BB%CE%AC%CE%B9%CE%BDEva_Klein%C3%89va_KleinKlein_%C3%89va%D4%B5%D5%BE%D5%A1_%D4%BF%D5%AC%D5%B5%D5%A1%D5%B5%D5%B6Eva_Klein%D0%9A%D0%BB%D1%8F%D0%B9%D0%BD,_%D0%95%D0%B2%D0%B0Eva_Klein%D0%9A%D0%BB%D1%8F%D0%B9%D0%BD,_%D0%95%D0%B2%D0%B0Eva_Klein%D0%95%D0%B2%D0%B0_%D0%9A%D0%BB%D1%8F%D0%B9%D0%BDQ249978
about
P26
SH2D1A expression reflects activation of T and NK cells in cord blood lymphocytes infected with EBV and treated with the immunomodulator PSKIL-21 imposes a type II EBV gene expression on type III and type I B cells by the repression of C- and activation of LMP-1-promoter.The MEC1 and MEC2 lines represent two CLL subclones in different stages of progression towards prolymphocytic leukemia.Type I interferons directly down-regulate BCL-6 in primary and transformed germinal center B cells: differential regulation in B cell lines derived from endemic or sporadic Burkitt's lymphoma.Latency type-dependent modulation of Epstein-Barr virus-encoded latent membrane protein 1 expression by type I interferons in B cells.Soluble factors produced by activated CD4+ T cells modulate EBV latency.Surveillance against tumors--is it mainly immunological?Cytokine mediated induction of the major Epstein-Barr virus (EBV)-encoded transforming protein, LMP-1.The proapoptotic function of SAP provides a clue to the clinical picture of X-linked lymphoproliferative diseaseLarge-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization.To the genesis of Burkitt lymphoma: regulation of apoptosis by EBNA-1 and SAP may determine the fate of Ig-myc translocation carrying B lymphocytes.Deficiency of the proapoptotic SAP function in X-linked lymphoproliferative disease aggravates Epstein-Barr virus (EBV) induced mononucleosis and promotes lymphoma development.Interaction of Epstein-Barr virus (EBV) with human B-lymphocytes.Restricted expression of EBV encoded proteins in in vitro infected CLL cells.T cells modulate Epstein-Barr virus latency phenotypes during infection of humanized miceThe role of DNA hypomethylation, histone acetylation and in vivo protein-DNA binding in Epstein-Barr virus-induced CD23 upregulation.Simultaneous detection of the two main proliferation driving EBV encoded proteins, EBNA-2 and LMP-1 in single B cells.STAT6 signaling pathway activated by the cytokines IL-4 and IL-13 induces expression of the Epstein-Barr virus-encoded protein LMP-1 in absence of EBNA-2: implications for the type II EBV latent gene expression in Hodgkin lymphoma.Concomitant increase of LMP1 and CD25 (IL-2-receptor alpha) expression induced by IL-10 in the EBV-positive NK lines SNK6 and KAI3.IL-10 can induce the expression of EBV-encoded latent membrane protein-1 (LMP-1) in the absence of EBNA-2 in B lymphocytes and in Burkitt lymphoma- and NK lymphoma-derived cell lines.EBV infection induces expression of the transcription factors ATF-2/c-Jun in B lymphocytes but not in B-CLL cells.In vitro EBV-infected subline of KMH2, derived from Hodgkin lymphoma, expresses only EBNA-1, while CD40 ligand and IL-4 induce LMP-1 but not EBNA-2.Upregulation of LMP1 expression by histone deacetylase inhibitors in an EBV carrying NPC cell line.cMyc-p53 feedback mechanism regulates the dynamics of T lymphocytes in the immune response.Cytomegalovirus-seropositive children show inhibition of in vitro EBV infection that is associated with CD8+CD57+ T cell enrichment and IFN-γ.p53 contributes to T cell homeostasis through the induction of pro-apoptotic SAP.Monocytes enhance cell proliferation and LMP1 expression of nasal natural killer/T-cell lymphoma cells by cell contact-dependent interaction through membrane-bound IL-15.The X-linked lymphoproliferative disease gene product SAP is expressed in activated T and NK cells.SH2D1A expression in Burkitt lymphoma cells is restricted to EBV positive group I lines and is downregulated in parallel with immunoblastic transformation.PSK and Trx80 inhibit B-cell growth in EBV-infected cord blood mononuclear cells through T cells activated by the monocyte products IL-15 and IL-12.Interferon γ is a strong, STAT1-dependent direct inducer of BCL6 expression in multiple myeloma cells.Activation of innate immunity by the leukotriene B 4 inhibits EBV induced B-cell transformation in cord-blood derived mononuclear cultures.Carbazole is a naturally occurring inhibitor of angiogenesis and inflammation isolated from antipsoriatic coal tar.The apoptosis modulating role of SAP (SLAM associated protein) contributes to the symptomatology of the X linked lymphoproliferative diseaseExpression of SH2D1A in five classical Hodgkin's disease-derived cell lines
P50
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P50
description
Hungarian-Swedish biologist
@en
Zweeds arts
@nl
biologa ungherese naturalizzata svedese
@it
doctoriță suedeză
@ro
dokter asal Swedia
@id
magyar származású svéd sejtbiológus, immunológus, onkológus, az MTA külső tagja
@hu
médica sueca
@ast
svensk professor
@sv
ungarisch-schwedische Medizinerin und Krebsforscherin
@de
Ιατρός και ερευνήτρια Ανοσολογίας του καρκίνου
@el
name
Eva Klein
@ast
Eva Klein
@ca
Eva Klein
@da
Eva Klein
@de
Eva Klein
@ee
Eva Klein
@en
Eva Klein
@es
Eva Klein
@fi
Eva Klein
@fo
Eva Klein
@fr
type
label
Eva Klein
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Eva Klein
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Eva Klein
@da
Eva Klein
@de
Eva Klein
@ee
Eva Klein
@en
Eva Klein
@es
Eva Klein
@fi
Eva Klein
@fo
Eva Klein
@fr
altLabel
Eva Fisher
@en
Eva Fisher
@it
Eva Klein
@hu
Eva Klein
@sq
Εύα Φίσερ
@el
prefLabel
Eva Klein
@ast
Eva Klein
@ca
Eva Klein
@da
Eva Klein
@de
Eva Klein
@ee
Eva Klein
@en
Eva Klein
@es
Eva Klein
@fi
Eva Klein
@fo
Eva Klein
@fr
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Wa34oAOK9hY
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0000 0000 7937 6430
P214
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n2014076326