PNU 74654 - CAS 113906-27-7
Category: Inhibitor
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Molecular Formula:
C19H16N2O3
Molecular Weight:
320.34
COA:
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Targets:
β-catenin
Description:
PNU 74654 inhibits the Wnt-β catenin pathway by blocking the interaction between β-catenin and TCF (T cell factor). Treatment of human adrenocortical cell lines with PNU 74654 significantly reduced expression of several Tcf/β-catenin target genes.
Purity:
≥99% by HPLC
Synonyms:
PNU 74654; PNU-74654; PNU74654; 2-Phenoxybenzoic acid-[(5-methyl-2-furanyl)methylene]hydrazide
Storage:
Store in a cool and dry place (or refer to the Certificate of Analysis).
MSDS:
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InChIKey:
JJEDWBQZCRESJL-DEDYPNTBSA-N
InChI:
InChI=1S/C19H16N2O3/c1-14-11-12-16(23-14)13-20-21-19(22)17-9-5-6-10-18(17)24-15-7-3-2-4-8-15/h2-13H,1H3,(H,21,22)/b20-13+
Canonical SMILES:
CC1=CC=C(O1)C=NNC(=O)C2=CC=CC=C2OC3=CC=CC=C3
1.β-Catenin/CBP-Dependent Signaling Regulates TGF-β-Induced Epithelial to Mesenchymal Transition of Lens Epithelial Cells.
Taiyab A;Korol A;Deschamps PA;West-Mays JA Invest Ophthalmol Vis Sci. 2016 Oct 1;57(13):5736-5747. doi: 10.1167/iovs.16-20162.
Purpose: ;Transforming growth factor-β-induced epithelial-mesenchymal transition (EMT) is one of the main causes of posterior capsular opacification (PCO) or secondary cataract; however, the signaling events involved in TGF-β-induced PCO have not been fully characterized. Here, we focus on examining the role of β-catenin/cyclic AMP response element-binding protein (CREB)-binding protein (CBP) and β-catenin/T-cell factor (TCF)-dependent signaling in regulating cytoskeletal dynamics during TGF-β-induced EMT in lens epithelial explants.;Methods: ;Rat lens epithelial explants were cultured in medium M199 in the absence of serum. Explants were treated with TGF-β2 in the presence or absence of the β-catenin/CBP interaction inhibitor, ICG-001, or the β-catenin/TCF interaction inhibitor, PNU-74654. Western blot and immunofluorescence experiments were carried out and analyzed.;Results: ;An increase in the expression of fascin, an actin-bundling protein, was observed in the lens explants upon stimulation with TGF-β, and colocalized with F-actin filaments. Inhibition of β-catenin/CBP interactions, but not β-catenin/TCF interactions, led to a decrease in TGF-β-induced fascin and stress fiber formation, as well as a decrease in the expression of known markers of EMT, α-smooth muscle actin (α-SMA) and matrix metalloproteinase 9 (MMP9).
2.Feminizing adrenocortical carcinoma - the source of estrogens production and the role of adrenal-gonadal de-differentiation.
Wu L;Xie J;Jiang L;Su T;Ye L;Zhou W;Jiang Y;Zhang C;Ning G;Wang W J Clin Endocrinol Metab. 2018 Jul 20. doi: 10.1210/jc.2018-00689. [Epub ahead of print]
Background: ;Feminizing adrenocortical carcinoma (ACC) is rare. The source of estrogens production and the underlying mechanism remain unclear.;Objective: ;In the present study, we investigated the source as well as molecular mechanism of estrogens production in feminizing ACC.;Methods: ;A total of 46 constitutive patients diagnosed with ACC were recruited in our single center. We described the clinical characters, steroid hormone profiling of peripheral and adrenal vein. In both feminizing ACC tissues and cell lines, we investigated the expression of steroidogenic biomarkers and β-catenin pathway by qPCR and immunohistochemical staining. The effect of Wnt inhibitors on the steroidogenesis were also analyzed in NCI-H295R cells.;Results: ;A total of 46 consecutive patients with ACC were analyzed and 25 were functional ACC. Four patients were diagnosed as feminizing ACC based upon feminizing manifestations, high levels of estradiol which was normalized after surgery and histological Weiss score. Gonadal steroidogenic biomarkers including CYP19A1, HSD17B3 and LHCGR were remarkably elevated in the feminizing ACC tissues. Adrenal veins sampling and LC-MS/MS suggested high CYP19A1 activities within the adrenal mass.
3.Juvenile ovary to testis transition in zebrafish involves inhibition of ptges.
Pradhan A;Olsson PE Biol Reprod. 2014 Aug;91(2):33. doi: 10.1095/biolreprod.114.119016. Epub 2014 Jun 11.
The sex differentiation mechanisms in zebrafish (Danio rerio) remains elusive, partly because of the absence of sex chromosomes but also because the process appears to depend on the synchrony of multiple genes and possibly environmental factors. Zebrafish gonadal development is initiated through the development of immature oocytes. Depending on multiple signaling cues, in about half of the individuals, the juvenile ovaries degenerate or undergo apoptosis to initiate testes development while the other half maintains the oogenic pathway. We have previously shown that activation of NFκB and prostaglandin synthase 2 (ptgs2) results in female-biased sex ratios. Prostaglandin synthase and prostaglandins are involved in multiple physiological functions, including cell survival and apoptosis. In the present study, we show that inhibition of ptgs2 by meloxicam results in male-biased sex ratios. On further evaluation, we observed that exposure with the prostaglandin D2 (PGD2) analogue BW-245C induced SRY-box containing gene 9a (sox9a) and resulted in male-biased sex ratios. On the other hand, prostaglandin E2 (PGE2) treatment resulted in female-biased sex ratios and involved activation of NFκB and the β-catenin pathway as well as inhibition of sox9.
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CAS 113906-27-7 PNU 74654

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