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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Interferon regulatory factor 8

ICSBP, IRF-8, interferon regulatory factor 8
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: IRF, Interferon Regulatory Factor-1, PU.1, CAN, MUM1
Papers on ICSBP
Positive Darwinian selection within interferon regulatory factor genes of Gymnocypris przewalskii (Cyprinidae) on the Tibetan Plateau.
New
Zhao et al., Xining, China. In Fish Shellfish Immunol, Feb 2016
Within this gene family, IRF3, IRF5, IRF7 and IRF8 contained positive selection sites.
IRF4 and IRF8 Act in CD11c+ Cells To Regulate Terminal Differentiation of Lung Tissue Dendritic Cells.
New
Kovats et al., Oklahoma City, United States. In J Immunol, Feb 2016
Conventional DC (cDC) subsets, CD11b(-) (cDC1s) or CD11b(+) (cDC2s), arise via distinct networks of transcription factors involving IFN regulatory factor 4 (IRF4) and IRF8, and are specialized for unique functional responses.
ROLES OF INTERFERON REGULATORY FACTORS IN CHRONIC MYELOID LEUKEMIA.
New
Vigneri et al., Catania, Italy. In Curr Cancer Drug Targets, Feb 2016
A growing body of evidence has suggested a role for both IRF4 and IRF8 in the pathogenesis of CML.
The Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) is Required for Termination of Emergency Granulopoiesis.
New
Eklund et al., United States. In J Biol Chem, Jan 2016
In this study, we found that the Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) was required to terminate emergency granulopoiesis.
Regulation of bifurcating B cell trajectories by mutual antagonism between transcription factors IRF4 and IRF8.
New
Impact
Singh et al., Cincinnati, United States. In Nat Immunol, Dec 2015
Here we identified a double-negative feedback loop between the transcription factors IRF4 and IRF8 that regulated the initial developmental bifurcation of activated B cells as well as the GC response.
Mediator kinase inhibition further activates super-enhancer-associated genes in AML.
New
Impact
Shair et al., Cambridge, United States. In Nature, Nov 2015
In AML cells, CA upregulated SE-associated genes with tumour suppressor and lineage-controlling functions, including the transcription factors CEBPA, IRF8, IRF1 and ETV6 (refs 6-8).
Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia.
New
Impact
Steidl et al., United States. In Nat Med, Oct 2015
AML progression was mediated by inhibition of expression of a PU.1-cooperating transcription factor, Irf8.
RORC1 Regulates Tumor-Promoting "Emergency" Granulo-Monocytopoiesis.
New
Impact
Sica et al., Milano, Italy. In Cancer Cell, Sep 2015
RORC1 orchestrates myelopoiesis by suppressing negative (Socs3 and Bcl3) and promoting positive (C/EBPβ) regulators of granulopoiesis, as well as the key transcriptional mediators of myeloid progenitor commitment and differentiation to the monocytic/macrophage lineage (IRF8 and PU.1).
Microglia recapitulate a hematopoietic master regulator network in the aging human frontal cortex.
Review
New
Ponting et al., Oxford, United Kingdom. In Neurobiol Aging, Aug 2015
We identified a subnetwork of transcription factors, including RUNX1, IRF8, PU.1, and TAL1, which are master regulators (MRs) for the age-dependent microglia module.
Host susceptibility to non-tuberculous mycobacterial infections.
Review
New
Holland et al., Bethesda, United States. In Lancet Infect Dis, Aug 2015
So far, at least seven autosomal mutations (in IL12B, IL12RB1, ISG15, IFNGR1, IFNGR2, STAT1, and IRF8) and two X-linked mutations (in IKBKG and CYBB), mostly presenting in childhood, have been reported to confer susceptibility to disseminated non-tuberculous mycobacterial infection.
Batf3 maintains autoactivation of Irf8 for commitment of a CD8α(+) conventional DC clonogenic progenitor.
New
Impact
Murphy et al., Saint Louis, United States. In Nat Immunol, Jul 2015
The transcription factors Batf3 and IRF8 are required for the development of CD8α(+) conventional dendritic cells (cDCs), but the basis for their actions has remained unclear.
Regulation of myelopoiesis by the transcription factor IRF8.
Review
New
Koizumi et al., Yokohama, Japan. In Int J Hematol, Apr 2015
Interferon regulatory factor-8 (IRF8) is a transcription factor expressed in hematopoietic cells, particularly in mononuclear phagocytes [monocytes/macrophages and dendritic cells (DCs)] and their progenitors.
NF-κB-Mediated Regulation of Osteoclastogenesis.
Review
New
Yao et al., Rochester, United States. In Endocrinol Metab (seoul), Apr 2015
However, these cytokines also activate NF-κB signaling that can limit osteoclast formation through the NF-κB signaling proteins, TRAF3 and p100, and the suppressors of c-Fos/NFATc1 signaling, IRF8, and RBP-J.
[Mechanisms underlying the pathogenesis of neuropathic pain revealing by the role of glial cells].
Review
New
Tsuda, In Nihon Shinkei Seishin Yakurigaku Zasshi, Feb 2015
Furthermore, interferon regulatory factor-8 (IRF8) and IRF5 are identified as microglial transcription factors whose expression is upregulated in spinal microglia after PNI, and the IRF8-IRF5 transcriptional cascade is the core process for shifting spinal microglia toward a state with high expression of P2X4 receptors.
A Single-Cell Gene-Expression Profile Reveals Inter-Cellular Heterogeneity within Human Monocyte Subsets.
Grip et al., Denmark. In Plos One, 2014
IRF8, CD40, CSF1R, NFⱪB1, RELA and TNF.
Interferon regulatory factor 8 integrates T-cell receptor and cytokine-signaling pathways and drives effector differentiation of CD8 T cells.
GeneRIF
Katz et al., Bethesda, United States. In Proc Natl Acad Sci U S A, 2012
Interferon regulatory factor 8 integrates T-cell receptor and cytokine-signaling pathways and drives effector differentiation of CD8 T cells.
Hematopoietic interferon regulatory factor 8-deficiency accelerates atherosclerosis in mice.
GeneRIF
Zernecke et al., München, Germany. In Arterioscler Thromb Vasc Biol, 2012
depletion of polymorphonuclear neutrophilic leukocytes in low-density lipoprotein receptor or apolipoprotein E-deficient mice with IRF8(-/-) or IRF8(-/-) apolipoprotein E-deficient bone marrow abrogated increased lesion formation
Notch-RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory macrophage polarization.
Impact
GeneRIF
Hu et al., New York City, United States. In Nat Immunol, 2012
The results defined a signaling network in which signaling via Notch-RBP-J and TLRs is integrated at the level of IRF8 synthesis. A mechanism was identified by which heterologous signaling pathways can regulate TLR-induced polarization of macrophages.
Identification of IRF8, TMEM39A, and IKZF3-ZPBP2 as susceptibility loci for systemic lupus erythematosus in a large-scale multiracial replication study.
GeneRIF
GENLES Network et al., Oklahoma City, United States. In Am J Hum Genet, 2012
Four additional susceptibility loci (IRF8, TMEM39A, IKZF3, and ZPBP2) for systemic lupus erythematosus were robustly established a multiethnic population (European, African American, Asian, Hispanic, Gullah, and Amerindian).
The leukemia-associated fusion protein Tel-platelet-derived growth factor receptor β (Tel-PdgfRβ) inhibits transcriptional repression of PTPN13 gene by interferon consensus sequence binding protein (Icsbp).
GeneRIF
Eklund et al., Chicago, United States. In J Biol Chem, 2012
interaction between Tel and Tel-PdgfRbeta decreases Tel/Icsbp/Hdac3 binding to the PTPN13 cis element, resulting in increased transcription.
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