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The vertical and paralleled Pu.1/Spi-b (show SPIB ELISA Kits) regulatory networks control the development of rostral blood island and ventral wall of dorsal aorta-borne macrophages by regulating Irf8.
Study reveals that specification of all macrophages requires irf8 during an early period of zebrafish hematopoiesis but not during the adult-phase. Also, Irf8 seems to have essential roles in host defense as well.
Irf8 is a critical determinant for neutrophil versus macrophage fate choice during zebrafish primitive myelopoiesis.
IRF8 is dispensable for induced pluripotent stem cell and embryonic stem cell differentiation into hemogenic endothelium and for endothelial-to-hematopoietic transition.
TP(thymidine phosphorylase (show TYMP ELISA Kits) ) curbed the expression of three proteins-IRF8, RUNX2 (show RUNX2 ELISA Kits), and osterix (show SP7 ELISA Kits). This downregulation was epigenetically driven: High levels of 2DDR, a product of TP secreted by myeloma cells, activated PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) signaling and increased the methyltransferase DNMT3A's expression
It findings provide evidence for an additional mechanism of epigenetic IRF8 silencing during osteoclastogenesis that likely works cooperatively with DNA methylation (show HELLS ELISA Kits), further emphasizing the importance of IRF8 as a negative regulator of osteoclastogenesis.
Data suggest that ubiquitin specific protease 4 (USP4 (show USP4 ELISA Kits)) interacts with interferon regulatory factor 8 (IRF8) and, by its Lys48-specific deubiquitinase/endopeptidase activity, stabilizes IRF8 protein levels in regulatory T-lymphocytes; USP4 (show USP4 ELISA Kits) and IRF8 are also expressed in helper T-lymphocytes.
these data indicate that human NK cells require IRF8 for development and functional maturation and that dysregulation of this function results in severe human disease, thereby emphasizing a critical role for NK cells in human antiviral defense.
down-regulation of IRF8 in the wound leads to impaired wound healing possibly through the regulation of macrophage function and apoptosis in skin wound.
IRF8 may contribute to the genetic susceptibility of Behcet's disease by regulating IRF8 expression and cytokine production.
IRF5 (show IRF5 ELISA Kits) and IRF8, two transcription factors with opposing functions, control TLR9 (show TLR9 ELISA Kits) signaling in human plasmacytoid dendritic cells.
cytarabine-induced upregulation of the IRF8 in leukemic cells involves increased levels of ZNF224, which can counteract the repressive activity of WT1 (show WT1 ELISA Kits) on the IRF8-promoter
Expression of WT1and IRF8 showed a moderate inverse correlation in acute myeloid leukemia (show BCL11A ELISA Kits) patients. WT1 (show WT1 ELISA Kits) can be used as an minimal residual disease marker, especially in patients without recurrent genetic abnormalities.
IRF8 does not play an essential intrinsic role in Th17 cell differentiation.
frequencies of antigen-experienced CD4 (show CD4 ELISA Kits)+CD11ahiCD49dhi cells that were CD44hiCD62L- were similar in MLN (show MLN ELISA Kits) of infected Irf8-/- and B6 mice, but the proportions of CD4 (show CD4 ELISA Kits)+GATA3 (show GATA3 ELISA Kits)+ and CD4 (show CD4 ELISA Kits)+IL-4 (show IL4 ELISA Kits)+ T cells were lower in infected Irf8-/- mice
Mysm1 enhanced function of the IRF2 and IRF8 promoters, suggesting that Mysm1 governs the IRFs for hematopoietic stem cell homeostasis.
results show that polymorphonuclear-myeloid-derived suppressor cells arise from a newly defined granulocyte progenitors (GP) stage within the bone marrow and that IRF8 levels (and/or their downstream target genes) in those GPs (show NBEAL2 ELISA Kits) guide their expansion or contraction
IRF8 differentially controls the survival.
IRF8 might play a role in restraining excess lymphocyte proliferation.
IRF8 controls Th1 immune response in Treg cells independent of T-bet.
The authors further identified a distinct molecular signature of F4/80(hi) and CD11b (show ITGAM ELISA Kits)(hi) macrophages and found that Irf8 was vital for macrophage maturation.
this study shows that myeloid-specific SIRT1 (show SIRT1 ELISA Kits) restrains pro-inflammatory processes by deacetylating IRF8
IRF8 was a target of miR (show MLXIP ELISA Kits)-451a in vitro and in vivo. The data indicate the function and a target of miR (show MLXIP ELISA Kits)-451a in SLE
Interferon consensus sequence-binding protein (ICSBP) is a transcription factor of the interferon (IFN) regulatory factor (IRF) family. Proteins of this family are composed of a conserved DNA-binding domain in the N-terminal region and a divergent C-terminal region that serves as the regulatory domain. The IRF family proteins bind to the IFN-stimulated response element (ISRE) and regulate expression of genes stimulated by type I IFNs, namely IFN-alpha and IFN-beta. IRF family proteins also control expression of IFN-alpha and IFN-beta-regulated genes that are induced by viral infection.
, interferon regulatory factor 8
, interferon regulatory factor 8-like
, interferon consensus sequence binding protein 1
, interferon consensus sequence-binding protein
, transcription factor ICSBP
, interferon consensus sequence binding protein