1. Eguchi J, Yan QW, Schones DE, Kamal M, Hsu CH, Zhang MQ, Crawford GE, Rosen ED. Interferon regulatory factors are transcriptional regulators of adipogenesis. Cell Metabolism. 2008; 7:86-94. PMCID:PMC2278019. 2. Xu Z, Yu S, Hsu CH, Eguchi J, Rosen ED. The orphan nuclear receptor chicken ovalbumin upstream promoter-transcription factor II is a critical regulator of adipogenesis. Proc Natl Acad Sci USA. 2008; 105: 2421-2426. PMCID:PMC2268152. 3. Mikkelsen TS, Xu Z, Zhang X, Wang L, Gimble JM, Lander ES, and Rosen ED. Comparative epigenomic analysis of murine and human adipogenesis. Cell. 2010. 143; 156-169. PMCID:PMC2950833. 4. Eguchi J, Wang X, Yu S, Kershaw EE, Chui PC, Dushay J, Estall JL, Klein U, Maratos-Flier E, and Rosen ED. Transcriptional control of adipose lipid handling by IRF4. Cell Metabolism. 2011; 13: 249-259. PMCID: PMC3063358. 5. Wrann CD, Eguchi J, Bozec A, Xu Z, Mikkelsen T, Gimble J, Nave H, Wagner EF, Ong S-E, and Rosen ED. FOSL2 promotes adipocyte-specific leptin gene ...

Duchenne muscular dystrophy (DMD) is a severe and progressive muscle-wasting disease caused by mutations in the dystrophin gene. Although dystrophin deficiency in myofiber triggers the diseases pathological changes, the degree of satellite cell (SC) dysfunction defines disease progression. Here, we have identified chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) hyperactivity as a contributing factor underlying muscular dystrophy in a dystrophin-deficient murine model of DMD. Ectopic expression of COUP-TFII in murine SCs led to Duchenne-like dystrophy in the muscles of control animals and exacerbated degenerative myopathies in dystrophin-deficient mice. COUP-TFII-overexpressing mice exhibited regenerative failure that was attributed to deficient SC proliferation and myoblast fusion. Mechanistically, we determined that COUP-TFII coordinated a regenerative program through combined regulation of multiple promyogenic factors. Furthermore, inhibition of COUP-TFII preserved SC ...

Duchenne muscular dystrophy (DMD) is a severe and progressive muscle-wasting disease caused by mutations in the dystrophin gene. Although dystrophin deficiency in myofiber triggers the diseases pathological changes, the degree of satellite cell (SC) dysfunction defines disease progression. Here, we have identified chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) hyperactivity as a contributing factor underlying muscular dystrophy in a dystrophin-deficient murine model of DMD. Ectopic expression of COUP-TFII in murine SCs led to Duchenne-like dystrophy in the muscles of control animals and exacerbated degenerative myopathies in dystrophin-deficient mice. COUP-TFII-overexpressing mice exhibited regenerative failure that was attributed to deficient SC proliferation and myoblast fusion. Mechanistically, we determined that COUP-TFII coordinated a regenerative program through combined regulation of multiple promyogenic factors. Furthermore, inhibition of COUP-TFII preserved SC ...

Gtf2ird1 (untagged) - Mouse general transcription factor II I repeat domain-containing 1 (Gtf2ird1), transcript variant 9, (10ug), 10 µg.

The general transcription factor II D (TFIID) is one of several general transcription factors that make up the RNA polymerase II preinitiation complex.[1] Before the start of transcription, the transcription factor II D (TFIID) complex, binds to the core promoter of the gene. TFIID is the first protein to bind to DNA during the formation of the pre-initiation transcription complex of RNA polymerase II (RNA Pol II). Binding of TFIID to the TATA box in the promoter region of the gene initiates the recruitment of other factors required for RNA Pol II to begin transcription. Some of the other recruited transcription factors include TFIIA, TFIIB, and TFIIF. Each of these transcription factors is formed from the interaction of many protein subunits, indicating that transcription is a heavily regulated process. Several of the TFIID subunits have been implicated in core promoter selectivity (Verrijzer and Tijan, 1996; Hampsey and Reinberg, 1997; Smale, 1997; Hahn, 1998).[2] ...

Alias: NR2F2, ARP1, ARP-1, COUP transcription factor II, COUP-TF II, COUP-TF2, COUP-TFII, COUPTFB, COUPTFII, COUP transcription factor 2, EAR3, NF-E3, SVP40, COUPTF-II, TFCOUP2 ...

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Rheumatoid arthritis (RA) is associated with a high prevalence of atherosclerosis. Recently increased levels of microparticles (MPs) have been reported in patients with RA. MPs could represent a link between autoimmunity and endothelial dysfunction by expressing tumor necrosis factor alpha (TNFα), a key cytokine involved in the pathogenesis of RA, altering endothelial apoptosis and autophagy. The aim of this study was to investigate TNFα expression on MPs and its relationship with endothelial cell fate. MPs were purified from peripheral blood from 20 healthy controls (HC) and from 20 patients with RA, before (time (T)0) and after (T4) 4-month treatment with etanercept (ETA). Surface expression of TNFα was performed by flow cytometry analysis. EA.hy926 cells, an immortalized endothelial cell line, were treated with RA-MPs purified at T0 and at T4 and also, with RA-MPs in vitro treated with ETA. Apoptosis and autophagy were then evaluated. RA-MPs purified at T0 expressed TNFα on their surface and this

The chicken ovalbumin upstream promoter transcription factors (COUP-TFs) are members from the steroid/thyroid hormone receptor superfamily and function in transcriptional regulation of a multitude of genes. of the ovalbumin gene (Bagchi et al., 1987; Pastorcic et al., 1986; Wang et Procyanidin B3 inhibitor Mouse monoclonal to Human Albumin al., 1987). It was found to bind an element (COUP) between C90 and C70 within the ovalbumin promoter that is much like thyroid and estrogen response elements (Pastorcic et al., 1986). The COUP-TF has also been shown to bind cis-elements involved in positive transcription rules in the rat insulin II (Hwung et al., 1988; Hwung et al., 1988b), chicken VLDL II (Wijnholds et Procyanidin B3 inhibitor al., 1988), and human being apolipoprotein AI and CIII genes (Ladias and Karathanasis, 1991). It was also reported to bind to bad regulatory elements in the proopiomelanocortin (Drouin et al., 1989a; Drouin et al., 1989b) and HIV-1 (Cooney et al., 1991) promoters. The ...

The sexual differentiation paradigm contends that the female pattern of the reproductive system is established by default because the male reproductive tracts (Wolffian ducts) in the female degenerate owing to a lack of androgen. Here, we discovered that female mouse embryos lacking Coup-tfII (chicken ovalbumin upstream promoter transcription factor II) in the Wolffian duct mesenchyme became intersex-possessing both female and male reproductive tracts. Retention of Wolffian ducts was not caused by ectopic androgen production or action. Instead, enhanced phosphorylated extracellular signal-regulated kinase signaling in Wolffian duct epithelium was responsible for the retention of male structures in an androgen-independent manner. We thus suggest that elimination of Wolffian ducts in female embryos is actively promoted by COUP-TFII, which suppresses a mesenchyme-epithelium cross-talk responsible for Wolffian duct maintenance. ...

B168 Nuclear receptors, the transcription factors regulated by ligands, have become major targets for drug discovery, including new drug development for chemotherapy. Orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor I (COUP-TFI) possesses the ability to either activate or repress the transcription of a diversity of target genes through undefined mechanisms. A proteomics-based, tandem affinity purification (TAP) procedure was used in this study to identify the component proteins of COUP-TFI complexes in mammalian cells. Several known proteins of transcriptional repressive complexes, including NCoR, HDAC1 and TIF1β/KAP-1, were found to co-purify with COUP-TFI, as were other transcriptional regulatory proteins, including the SWI/SNF family member Brahma, and its associated factors BAF155 and BAF170. Proteins not previously implicated in transcriptional regulation were also found to co-purify with COUP-TFI including the DNA repair protein DDB1, a pro-apoptotic ...

Sugiyama T, Wang JC, Scott DK, Granner DK (Feb 2000). Transcription activation by the orphan nuclear receptor, chicken ovalbumin upstream promoter-transcription factor I (COUP-TFI). Definition of the domain involved in the glucocorticoid response of the phosphoenolpyruvate carboxykinase gene. The Journal of Biological Chemistry. 275 (5): 3446-54. doi:10.1074/jbc.275.5.3446. PMID 10652338 ...

In the mosquito Aedes aegypti, vitellogenesis is activated via an ecdysteroid hormonal cascade initiated by a blood meal. The functional ecdysone receptor is a heterodimer composed of the ecdysone receptor (EcR) and ultraspiracle, the homolog of the retinoid X receptor. The precise tuning of this hormonal response requires participation of both positive and negative transcriptional regulators. In Drosophila, Svp, a homolog of chicken ovalbumin upstream promoter transcription factor (COUP-TF), inhibits ecdysone receptor complex-mediated transactivation in vitro and in vivo. Here we report the cloning and characterization of the Svp homolog in mosquito Aedes aegypti, AaSvp. It possesses a high degree of amino acid sequence similarity to the members of the COUP-TF/Svp subfamily. AaSvp transcripts and protein are present in the fat body at high levels from the state of arrest to about 60 h post blood meal. AaSvp binds strongly to a variety of direct repeats of the sequence AGGTCA, but weakly to ...

Sigma-Aldrich offers abstracts and full-text articles by [Jae Hyeon Kim, Jin-Kyu Kim, Eun-Kyung Ahn, Hye-Jin Ko, Young-Rak Cho, Choong Hyun Lee, Yong Kee Kim, Gyu-Un Bae, Joa Sub Oh, Dong-Wan Seo].

Regulation of retinoic acid-induced inhibition of AP-1 activity by orphan receptor chicken ovalbumin upstream promoter-transcription factor

Biology of Reproduction contains original scientific research on a broad range of topics in the field of reproductive biology, as well as minireviews.

Members of the evolutionarily conserved family of the chicken ovalbumin upstream promoter transcription factor NR2F/COUP-TF orphan receptors have been implicated in lymphocyte biology, ranging from activation to differentiation and elicitation of immune effector functions. In particular, a CD4+ T cell intrinsic and non-redundant function of NR2F6 as a potent and selective repressor of the transcription of the pro-inflammatory cytokines interleukin (Il) 2, interferon y (ifng) and consequently of T helper (Th)17 CD4+ T cell-mediated autoimmune disorders has been discovered. NR2F6 serves as an antigen receptor signaling threshold-regulated barrier against autoimmunity where NR2F6 is part of a negative feedback loop that limits inflammatory tissue damage induced by weakly immunogenic antigens such as self-antigens. Under such low affinity antigen receptor stimulation, NR2F6 appears as a prototypical repressor that functions to

COUP Transcription Factors: A sub-family of steroid receptor-related orphan nuclear receptors that have specificity for a variety of DNA sequences related to AGGTCA. COUP transcription factors can heterodimerize with a variety of factors including RETINOIC ACID RECEPTORS; THYROID HORMONE RECEPTORS; and VITAMIN D RECEPTORS.

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J:244916 Zhao F, Franco HL, Rodriguez KF, Brown PR, Tsai MJ, Tsai SY, Yao HH, Elimination of the male reproductive tract in the female embryo is promoted by COUP-TFII in mice. Science. 2017 Aug 18;357(6352):717-720 ...

Differentiation of arteries and veins is essential for the development of a functional circulatory system. In vertebrate embryos, genetic manipulation of Notch signaling has demonstrated the importance of this pathway in driving artery endothelial cell differentiation. However, when and where Notch activation occurs to affect endothelial cell fate is less clear. Using transgenic zebrafish bearing a Notch-responsive reporter, we demonstrate that Notch is activated in endothelial progenitors during vasculogenesis prior to blood vessel morphogenesis and is maintained in arterial endothelial cells throughout larval stages. Furthermore, we find that endothelial progenitors in which Notch is activated are committed to a dorsal aorta fate. Interestingly, some arterial endothelial cells subsequently downregulate Notch signaling and then contribute to veins during vascular remodeling. Lineage analysis, together with perturbation of both Notch receptor and ligand function, further suggests several distinct

LXR α 0h 4h 8h 18h 1D 2D 3D 4D 5D 6D 7D 8D h 2d d Induction MediumDifferentiation Medium NR Expression during Adipogenesis of 3T3-L1 Cells (2) Fu et al., Mol. Endo. 19: 2437 (2005) Nur77 PPAR γ NUR77 LXR  PPAR 