Representing With the NK cells is 2-3% of total splenocytes. Effector function of NK cells and wild-type PLZF-/ – mice M was investigated by testing their cytolytic activity against NK-sensitive line t of YAC-1 target cells. After treatment with poly, which activates NK cells through IFNsignaling, PLZF-/ – NK cells have in their R ability to lyse 2-Methoxyestradiol 362-07-2 spontaneously YAC-1 cells disabled. Furthermore, when used in vivo with IFN, the ability of PLZF-F / activated – NK cells after lysis YAC-1 target cells was also significantly reduced. These results show that NK cells PLZF effector function is required and to regulate also the fact that PLZF, the expression of target genes in NK cytolytic activity t involved.
Such as cytokine-induced activation of NK 2-Methoxyestradiol HIF inhibitor cells leads to a drastic Erh Hung examined the expression of granzyme B, we the F Ability of poly and IL-2 to induce the protein expression in murine spleen-granzyme B NK cells. The Mice Were injected intraperitoneally with PBS or were injected several times and spleen NK cells analyzed after 24 hours for granzyme B expression by FACS. The spleen of mice wild-type M, which had been injected with Poly, a significantly higher percentage of hours of NK cells positive for GzmB the spleen of PLZF-/ – mice M. The erm IGTE GzmB is compatible with a reduced F Ability to lyse target cells. The activation of NK cells in vitro with IL-2 induced Equivalent amounts of GzmB either genotype. Therefore, the r Of the PLZF in the induction of IFN GzmB, t like than other cytokines.
PLZF directly regulates the promoters of a subset of ISGs as n To search results we have investigated the mechanism obtained by the PLZF Hte define the expression of a specific subset of ISGs. Treatment of U937T: PLZF45 cells with the transcription actinomycin D suggested that the induction of ISG of PLZF selected hlt re prim in transcription. Promoter regions of PLZF-regulated transcription factors and rsad2 IFIT2, were the luciferase activity t was fused to IFN-treatment measure. The overexpression of PLZF in RCC1 and ACHN cells resulted in a dose-dependent Independent induction of reporter promoters. This effect was enhanced by IFN treatment. Therefore, the induction of the promoter rsad2 in cells with reduced expression of RNA interference PLZF was adversely Chtigt. Reporter constructs confirm to the need to put together ISRE and PLZF binding sites in promoters of PLZF-regulated ISGs.
PLZF45 cell lines: A direct mapping of PLZF with promoters and rsad2 IFIT2 was demonstrated by chromatin Immunopr zipitation tests in RCC1 and U937T. In addition, the association of PLZF and rsad2 IFIT2 strong promoters of IFN-treatment improved. Active IFN PLZF increased the observed relationship Hter IFN PLZF with some ISG promoters k Can direct post-translational modification of PLZF, and / or Ver Change the transcriptional cofactors occur. Examine old, was PLZF from controlled U937T and the IFN-treated immunpr zipitiert: PLZF45 cells and the state of acetylation or phosphorylation of the protein was examined by Western blot. Although acetylation was reported to be important for DNA binding of PLZF is that no Changes in the acetylation state detected.
It has been established that are correlated with phosphorylated serine and tyrosine with tyrosine phosphorylation of PLZF with temporal processing with IFN. PLZF code for two types of conserved Dom ne, a BTB at the N-terminal repeats and nine Zinkfingerdom NEN To the C-terminus. BTB high as a cathedral Were revealed and protein essential for homodimerization � �� rotein interaction, w We hlten on Residues Focus walls in this area. By aligning the amino Acid sequence of PLZF BTB with different regions of other proteins and by analysis with Pr Diction programs were identified some potential phosphorylated residues in the range of PLZF BTB with residues previously identified as critical for function as a transcriptional repressor PLZF. Residues Walls mutated in PLZF