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anti-Human IRF8 Anticorps:
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Human Polyclonal IRF8 Primary Antibody pour ELISA, WB - ABIN1002562
Weisz, Marx, Sharf, Appella, Driggers, Ozato, Levi: Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes. dans The Journal of biological chemistry 1993
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Human Polyclonal IRF8 Primary Antibody pour WB - ABIN541245
Nelson, Marks, Driggers, Ozato: Interferon consensus sequence-binding protein, a member of the interferon regulatory factor family, suppresses interferon-induced gene transcription. dans Molecular and cellular biology 1993
Show all 3 Pubmed References
Cow (Bovine) Polyclonal IRF8 Primary Antibody pour WB - ABIN2777225
Ye, Wang, Wang, Wang, Song, Hou, Zhou, Li, Ho: CD56+ T cells inhibit hepatitis C virus replication in human hepatocytes. dans Hepatology (Baltimore, Md.) 2009
Human Polyclonal IRF8 Primary Antibody pour WB - ABIN6682139
Yu, Liu, Zhu, Zhu, Lv, Wang, Wang, Peng: The Expression of Interferon Regulatory Factor 8 in Human Periapical Lesions. dans Journal of endodontics 2019
Human Polyclonal IRF8 Primary Antibody pour ELISA, WB - ABIN561405
Conzelmann, Wagner, Hildebrandt, Rodionova, Hess, Zota, Giese, Falk, Ho, Dreger, Hecker, Luft: IFN-? activated JAK1 shifts CD40-induced cytokine profiles in human antigen-presenting cells toward high IL-12p70 and low IL-10 production. dans Biochemical pharmacology 2010
The vertical and paralleled Pu.1/Spi-b 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.
This paper suggests that IRF4 and IRF8 are important in the counter-balancing mechanisms controlling differentiation of plasma cells in myasthenia gravis.
interferon consensus sequence-binding protein upregulates transforming growth factor-beta type I receptor (TGF-beta RI) expression by binding to nucleotides -216/-211 (GGXXTC) in the TGF-beta RI promoter, which resulted in increased tumorigenicity and tumor progression in human osteosarcoma cells.
Our work complements existing data to indicate an important role for IRF8 suppression in APL pathogenesis.
data supports a role for regulation of these genes in mononuclear phagocytic cells by vitamin D as contributing to autoimmunity
These findings identified a novel function of IRF-8 in regulating articular cartilage matrix destruction by promoting the expression of MMP-13.
Exogenous expression of IRF8 in the silenced or downregulated lung cancer cell lines restored the sensitivity of lung cancer cells to apoptosis, and arrested cells at the G0/G1 phase. IRF8 bound to the T-cell factor/lymphoid enhancer factor (TCF /LEF) promoter, thus repressing beta-catenin nuclear translocation and its activation.
Study shows that hypermethylation of IRF8 associated with decreased mRNA expression in dendritic cells confers risk to VKH disease.
IRF8 upregulation in tumor cells inhibited the generation of Th17 cells in vitro, and this may be mediated by the downregulation of RORgammat. we found that a high level of IRF8 in the DLBCL tumor microenvironment was a predictor of poor survival in DLBCL patients.
These findings identify IRF8 as a novel tumor suppressor regulating IFN-gamma/STAT1 signaling and beta-catenin signaling in breast cancer.
Irf8 induction, but not its knockdown, decreased APL leukemogenic potential through driving monocytic maturation.
Total cellular protein presence of the transcription factor IRF8 does not necessarily correlate with its nuclear presence.
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 ) curbed the expression of three proteins-IRF8, RUNX2, and osterix. This downregulation was epigenetically driven: High levels of 2DDR, a product of TP secreted by myeloma cells, activated PI3K/AKT 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, further emphasizing the importance of IRF8 as a negative regulator of osteoclastogenesis.
Data suggest that ubiquitin specific protease 4 (USP4) interacts with interferon regulatory factor 8 (IRF8) and, by its Lys48-specific deubiquitinase/endopeptidase activity, stabilizes IRF8 protein levels in regulatory T-lymphocytes; USP4 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 and IRF8, two transcription factors with opposing functions, control TLR9 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 on the IRF8-promoter
early expression of the key transcription factor IRF8 changes chromatin states in otherwise multipotent progenitors, biasing their fate decision toward dendritic cells
myeloid-derived suppressor cells -IL-10-STAT3-DNMT3b-IRF8 pathway as a link between chronic inflammation and colon cancer initiation.
IRF8 deletion in dendritic cells significantly reduces the development of atherosclerosis.
gene network analysis and conditional deletion revealed IRF8 as a master regulator that drives the maturation and diversity of brain macrophages
Although Irf8(-/-) mononuclear phagocyte progenitors, including monocyte-dendritic cell progenitors , displayed grossly normal gene expression patterns, their enhancer landscapes resembled that of an upstream progenitor population.
work identifies that mTOR is an intrinsic master for monocyte/macrophage development at the early stages through regulating STAT5-IRF8-dependent CD115-expressing pathway.
IRF8 is a critical regulator of NAIPs and NLRC4 inflammasome activation for defense against bacterial infection.
Sca1(+)Lin(-)CD117(-) mouse bone marrow-derived mesenchymal stem cells regulate immature dendritic cell maturation by inhibiting TLR4-IRF8 signaling via the Notch-RBP-J pathway.
These findings identify the function and cell-type-specific regulation of IRF8 in NK-cell-mediated antiviral immunity
breast and pancreatic tumor-produced granulocyte-stimulating factor downregulates interferon regulatory factor-8 in conventional dendritic cells (cDC) progenitors, and thus results in reduced cDC1 development
Study shows that IRF8 is required for Th9 differentiation in vitro and in vivo. IRF8 functions through a transcription factor complex consisting of IRF8, IRF4, PU.1 and BATF, which binds to DNA and boosts Il9 transcription.
Expression of IRF-8 is significantly elevated in the microglia of AD mice. Silencing of IRF-8 abolished Abeta1-40-induced microglia activation.
DNA methylation plays a protective role in cisplatin-induced acute kidney injury by regulating specific genes, such as Irf8.
IRF8 does not play an essential intrinsic role in Th17 cell differentiation.
frequencies of antigen-experienced CD4+CD11ahiCD49dhi cells that were CD44hiCD62L- were similar in MLN of infected Irf8-/- and B6 mice, but the proportions of CD4+GATA3+ and CD4+IL-4+ 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 guide their expansion or contraction
IRF8 differentially controls the survival.
IRF8 might play a role in restraining excess lymphocyte proliferation.
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