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anti-Human IRF4 Antikörper:
anti-Mouse (Murine) IRF4 Antikörper:
anti-Rat (Rattus) IRF4 Antikörper:
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Dog (Canine) Polyclonal IRF4 Primary Antibody für WB - ABIN2780429
Han, Kraft, Nan, Guo, Chen, Qureshi, Hankinson, Hu, Duffy, Zhao, Martin, Montgomery, Hayward, Thomas, Hoover, Chanock, Hunter: A genome-wide association study identifies novel alleles associated with hair color and skin pigmentation. in PLoS genetics 2008
Mouse (Murine) Polyclonal IRF4 Primary Antibody für ICC, IHC - ABIN1859474
Bakalar, Joffe, Schmid, Son, Podolski, Fletcher: Size-Dependent Segregation Controls Macrophage Phagocytosis of Antibody-Opsonized Targets. in Cell 2018
Human Polyclonal IRF4 Primary Antibody für ELISA, ICC - ABIN4327575
Nagel, Pommerenke, Meyer, Kaufmann, MacLeod, Drexler: NKL homeobox gene MSX1 acts like a tumor suppressor in NK-cell leukemia. in Oncotarget 1970
IRF4 polymorphism is associated with rheumatoid arthritis.
may represent a therapeutic target in adult T-cell leukemia(ATL) because ATL cells select for a mutant of IRF4 with higher nuclear expression and transcriptional activity, and overexpression of IRF4 induces the expansion of T lymphocytes in vivo
The results indicate that an inherited functional variant in IRF4 may independently predict Breslow thickness - the most important prognostic indicator for melanoma.
High IRF4 expression is associated with melanoma.
IRF4 pathway is required for functional development of type 1 regulatory T cells.
In Pakistani population, the frequency of GCB type DLBCL [diffuse large B cell lymphoma ]expressing CD10 and BCL6 is 37.5%, and non- GCB type DLBCL [diffuse large B cell lymphoma ] expressing MUM1 is 62.5%.
Study confirmed a significant role for IRF4 rs12203592 and SLC45A2 rs16891982 in the risk of cutaneous squamous cell carcinoma development in organ transplant recipients.
IRF4 is overexpressed in human non-small cell lung cancer and activates the Notch signaling pathway.
IRF4 signaling is essential for activin A induced regulatory T cells that restrain asthmatic responses.
The data indicate that USP4 interacts with and deubiquitinates IRF4, and also stabilizes IRF4 protein and promotes IRF4 function to facilitate IL-4 expression in Th2 cells, which may be related to the pathological process of rheumatic heart disease.
IRF4 is an independent prognostic factor for general MM patients.
Data show that the host transcript of miR-223, linc-223, as a novel functional long non-coding RNA (lncRNA) and induces interferon regulatory factor 4 (IRF4) expression in acute myeloid leukemia.
Evidence for an essential role of Notch signaling in the development of chronic lymphocytic leukemia (CLL) and establish IRF4 as a critical regulator of Notch signaling during CLL development.
These results show that significantly increased levels of FOXO3, IRF4, and xIAP mRNA in Chinese HIV-1-infected patients.
Mechanistically, we found that BETi-mediated inhibition of cMYC correlates with the upregulation of miR-125b-5p and the downregulation of the cMYC/miR-125b-5p target gene IRF4, a transcriptional repressor of MICA.
BCL7A, BRWD3, and AUTS2 demonstrate significantly higher mutation frequencies among AA cases. These genes are all involved in translocations in B-cell malignancies. Moreover, we detected a significant difference in mutation frequency of TP53 and IRF4 with frequencies higher among CA cases. Our study provides rationale for interrogating diverse tumor cohorts to best understand tumor genomics across populations.
IRF4 protects arteries against neointima formation by promoting the expression of KLF4 by directly binding to its promoter.
We propose that the Irf4 locus functions as the "reader" of TCR signal strength, and in turn, concentration-dependent activity of Irf4 "writes" T helper fate choice.
PU.1-induced apoptosis in myeloma cells is associated with IRF4 downregulation and subsequent IRF7 upregulation.
GM-CSF can mediate inflammation and pain by regulating IRF4-induced CCL17 production
These results suggest that IRF4 regulates the clonal expansion of CD8(+) T cells at least in part via the AKT signaling pathway. Moreover, IRF4 regulates the homeostatic proliferation of naive CD8(+) T cells, whereas the maintenance of memory CD8(+) T cells is IRF4-independent.
Data show that interferon regulatory factor 1 (IRF1) occupancy correlates with decreased interferon regulatory factor 4 (IRF4) abundance, suggesting an IRF1-IRF4-binding competition at the interleukin 9 (Il9) locus.
Furthermore, chromatin immunoprecipitation (ChIP) followed by luciferase assays revealed direct binding of Foxo1 to both the Il9 and Irf4 promoters and induces their transactivation.
MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression
study identifies IRF4 as central regulator of TH1 responses and cellular metabolism. We propose that this function of IRF4 is fundamental for the initiation and maintenance of all TH cell responses.
Nur77 suppresses CD4(+) T cell proliferation and uncover a suppressive role for Irf4 in TH2 polarization; halving Irf4 gene-dosage leads to increases in GATA3(+) and IL-4(+) cells.
Muramyl dipeptide reduces fat inflammation and liver insulin resistance via NOD2. NOD1-activating muropeptides exacerbate glucose intolerance. IRF4 dictates insulin-sensitizing effects of NOD2, but not NOD1, muropeptides.
Young mice had higher levels of IRF4 in the ischemic brains, suggesting that aging has a significant influence on stroke outcomes in mice, which is probably mediated by age-specific inflammatory responses.
IRF4 is highly induced in graft-infiltrating T cells and is required for heart transplant rejection.
The findings indicate that IRF4 functions as a central node in a TCR-responsive transcriptional circuit that establishes and sustains T cell exhaustion during chronic viral infection.
RHS6 is a critical regulatory element for allergic airway inflammation and for coordinate regulation of Th2 cytokine genes by recruiting GATA3, SATB1, and IRF4.
this study shows that epicutaneous sensitization to house dust mite allergen requires interferon regulatory factor 4-dependent dermal dendritic cells
Cell fate and metabolic state are linked by transcriptional regulators, such as IRF4 and FoxO1, with dual roles in lineage and metabolic choice. Instructing some cells to utilize nutrients for anabolism and differentiation while other cells catabolically self-digest and self-renew may enable growth and repair in metazoa.
Here the authors show that concomitant loss of Tet2 and Tet3 in mice at early B cell stage blocked the pro- to pre-B cell transition in the bone marrow, decreased Irf4 expression and impaired the germline transcription and rearrangement of the Igkappa locus.
Data show that Fos-Related Antigen-2 (Fra-2) is a key upstream regulator of forkhead box O1 (Foxo1) and interferon regulatory factor 4 (Irf4) expression and influences proliferation and differentiation of B cells at multiple stages.
MTORC2 operated in parallel with the IL-4Ralpha-Stat6 pathway.
IRF4 mRNA and protein expression was remarkably suppressed during the development of myeloid-derived suppressor cells in the tumor microenvironment. IRF4 expression in MDSCs can modulate their activity to inhibit T cell proliferation through IL-10 production and ROS generation, and myeloid-specific deletion of IRF4 leads to the increase of MDSC differentiation. IRF4 reduction induced by tumors can increase MDSC numbers.
IRF4a and IRF4b displayed a distinct tissue expression pattern, embryonic stages expression and inducible expression in vivo and in vitro, suggesting that IRF4 paralogues might play different roles in immune system.
The protein encoded by this gene belongs to the IRF (interferon regulatory factor) family of transcription factors, characterized by an unique tryptophan pentad repeat DNA-binding domain. The IRFs are important in the regulation of interferons in response to infection by virus, and in the regulation of interferon-inducible genes. This family member is lymphocyte specific and negatively regulates Toll-like-receptor (TLR) signaling that is central to the activation of innate and adaptive immune systems. A chromosomal translocation involving this gene and the IgH locus, t(6\;14)(p25\;q32), may be a cause of multiple myeloma. Alternatively spliced transcript variants have been found for this gene.
lymphocyte-specific interferon regulatory factor
, multiple myeloma oncogene 1
, PU.1 interaction partner
, Sfpi1/PU.1 interaction partner
, transcriptional activator PIP
, interferon regulatory factor 4
, Interferon regulatory factor 4
, PWWP domain-containing protein MUM1
, melanoma associated antigen (mutated) 1