Anti-FOXO3 polyclonal antibody (DPAB-DC1045)

Mouse anti-Human FOXO3 (aa 361-460) polyclonal antibody for WB, ELISA


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Alternative Names
FOXO3; forkhead box O3; FOXO2; AF6q21; FKHRL1; FOXO3A
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Product Background

AKT phosphorylates targets in the nucleus; AMPK signaling pathway; BDNF signaling pathway; Chemokine signaling pathway


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Dysregulation of FOXO transcription factors in Epstein-Barr virus-associated gastric carcinoma


Authors: Liu, Wen; Song, Ying-ying; Wang, Jia-yi; Xiao, Hua; Zhang, Yan; Luo, Bing

Epstein-Barr virus (EBV) infection is associated with the development of gastric cancer (GC). Forkhead box class O (FOXO) transcription factors play important roles in tumor suppression. This study aims to investigate the interplay between EBV and FOXOs in EBV-associated GC (EBVaGC). The results showed that EBV infection of GC cells led to the downregulation of FOXO1 by the inhibition of its mRNA and protein expression. FOXO3 protein is repressed by EBV infection. FOXO4 mRNA is upregulated in EBV-positive cell lines, while its protein expression is downregulated. FOXO1, FOXO3 and FOXO4 proteins are upregulated following PI3K inhibition in GT39 cells, confirming that they are partially suppressed by the PI3K/AKT pathway. However, the upregulation of FOXO1 and FOXO3 by single transfection with LMP1 or LMP2A implies that the dysregulation of FOXOs in EBVaGC is affected by various EBV latent genes and that PI3K/AKT signaling is not the only mechanism of FOXO regulation.

Thymosin-beta 4 Mediates Hepatic Stellate Cell Activation by Interfering with CircRNA-0067835/miR-155/FoxO3 Signaling Pathway


Authors: Zhu, Lili; Ren, Tingting; Zhu, Zixin; Cheng, Mingliang; Mou, Qiuju; Mu, Mao; Liu, Yongmei; Yao, Yumei; Cheng, Yiju; Zhang, Baofang; Cheng, Zhuo

Background/Aims: Hepatic stellate cells (HSCs) are the primary cell type responsible for liver fibrosis. Our study proved that thymosin beta 4 (T beta 4) has anti-fibrogenic effects in HSCs through PI3K/AKT pathway. However, the underlying mechanisms are not fully elucidated. Circular RNAs (circRNAs) play important roles in fine-tuning gene expression and are often deregulated in cancers. However, the expression profile and clinical significance of in liver fibrosis is still unknown. Therefore, we hypothesize that T beta 4 influences circRNAs in liver fibrosis. Methods: Circular RNA microarray was conducted to identify T beta 4-related circRNAs. Pathway analysis and miRNA response elements analysis was conducted to predict the potential roles of differentially expressed circRNAs in liver fibrosis. CCK8 assays and flow cytometric assays were conducted to clarify the role of circRNA in liver fibrosis. Bioinformatics analysis and in vitro experiments were conducted to clarify the mechanism of circRNA-mediated gene regulation in liver fibrosis. Results: A total of 644 differentially expressed circRNAs were identified between the T beta 4-depleted LX-2 cells and the control LX2 cells. The expression of circRNA-0067835 was significantly increased in the T beta 4-depleted LX-2 cells compared with control. Knockdown of circRNA-0067835 observably decreased LX-2 cell proliferation by causing G1 arrest and promoting apoptosis. Bioinformatics online programs predicted that circRNA-0067835 acted as miR-155 sponge to regulate FOXO3a expression, which was validated using luciferase reporter assay. Conclusion: Our experiments showed that circRNA-0067835 regulated liver fibrosis progression by acting as a sponge of miR-155 to promote FOXO3a expression, indicating that circRNA-0067835 may serve as a potential therapeutic target for patients with liver fibrosis. (C) 2018 The Author(s) Published by S. Karger AG, Basel

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