Anti-FOXO3 polyclonal antibody (CPBT-66327GF)

Goat anti-Human FOXO3 (C-terminal) polyclonal antibody for ELISA, WB

Specifications


Host Species
Goat
Antibody Isotype
IgG
Species Reactivity
Human, Dog, Mouse, Rat
Immunogen
Peptide sequence C-GAKQASSQSWVPG corresponding to the C-terminal region of FOXO3A (NP_001446.1; NP_963853.1).
Conjugate
Unconjugated

Applications


Application Notes
ELISA: 1/32,000; Western Blot: 0.5 - 2.0ug/ml;
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
FOXO3; forkhead box O3; FOXO2; AF6q21; FKHRL1; FOXO3A
Entrez Gene ID
UniProt ID
O43524

Product Background


Pathway
AKT phosphorylates targets in the nucleus; AMPK signaling pathway; Adaptive Immune System; BDNF signaling pathway; Chemokine signaling pathway; Class I PI3K signaling events; Class I PI3K signaling events mediated by Akt; Constitutive PI3K/AKT Signaling in Cancer;

Citations


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Custom Antibody Labeling


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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References


Tubular beta-catenin and FoxO3 interactions protect in chronic kidney disease

JCI INSIGHT

Authors: Nlandu-Khodo, Stellor; Osaki, Yosuke; Scarfe, Lauren; Yang, Haichun; Phillips-Mignemi, Melanie; Tonello, Jane; Saito-Diaz, Kenyi; Neelisetty, Surekha; Ivanova, Alla; Huffstater, Tessa; McMahon, Robert; Taketo, M. Mark; DeCaestecker, Mark; Kasinath, Balakuntalam; Harris, Raymond C.; Lee, Ethan; Gewin, Leslie S.

The Wnt/beta-catenin signaling pathway plays an important role in renal development and is reexpressed in the injured kidney and other organs. beta-Catenin signaling is protective in acute kidney injury (AKI) through actions on the proximal tubule, but the current dogma is that Wnt/beta-catenin signaling promotes fibrosis and development of chronic kidney disease (CKD). As the role of proximal tubular beta-catenin signaling in CKD remains unclear, we genetically stabilized (i.e., activated) beta-catenin specifically in murine proximal tubules. Mice with increased tubular beta-catenin signaling were protected in 2 murine models of AKI to CKD progression. Oxidative stress, a common feature of CND, reduced the conventional T cell factor/lymphoid enhancer factor-dependent beta-catenin signaling and augmented FoxO3-dependent activity in proximal tubule cells in vitro and in vivo. The protective effect of proximal tubular beta-catenin in renal injury required the presence of FoxO3 in vivo. Furthermore, we identified cystathionine gamma-Iyase as a potentially novel transcriptional target of beta-catenin/FoxO3 interactions in the proximal tubule. Thus, our studies overturned the conventional dogma about beta-catenin signaling and CKD by showing a protective effect of proximal tubule beta-catenin in CKD and identified a potentially new transcriptional target of beta-catenin/FoxO3 signaling that has therapeutic potential for CKD.

FLT3 inhibition upregulates HDAC8 via FOXO to inactivate p53 and promote maintenance of FLT3-ITD+ acute myeloid leukemia

BLOOD

Authors: Long, Jun; Jia, Ming-Yuan; Fang, Wei-Yue; Chen, Xin-Jie; Mu, Li-Li; Wang, Zhong-Yu; Shen, Yan; Xiang, Ru-Fang; Wang, Li-Ning; Wang, Ling; Jiang, Chuan-He; Jiang, Jie-Ling; Zhang, Wen-Jun; Sun, Yi-Dan; Chang, Li; Gao, Wen-Hui; Wang, Ying; Li, Jun-Min; Hong, Deng-Li; Liang, Ai-Bin; Hu, Jiong

Internal tandem duplication (ITD) mutations within the FMS-like receptor tyrosine kinase-3 (FLT3) can be found in up to 25% to 30% of acute myeloid leukemia (AML) patients and confer a poor prognosis. Although FLT3 tyrosine kinase inhibitors (TKIs) have shown clinical responses, they cannot eliminate primitive FLT3-ITD+ AML cells, which are potential sources of relapse. Therefore, elucidating the mechanisms underlying FLT3-ITD+ AML maintenance and drug resistance is essential to develop novel effective treatment strategies. Here, we demonstrate that FLT3 inhibition induces histone deacetylase 8 (HDAC8) upregulation through FOXO1- and FOXO3-mediated transactivation in FLT3-ITD+ AML cells. Upregulated HDAC8 deacetylates and inactivates p53, leading to leukemia maintenance and drug resistance upon TKI treatment. Genetic or pharmacological inhibition of HDAC8 reactivates p53, abrogates leukemia maintenance, and significantly enhances TKI-mediated elimination of FLT3-ITD+ AML cells. Importantly, in FLT3-ITD+ AML patient-derived xenograft models, the combination of FLT3 TKI (AC220) and an HDAC8 inhibitor (22d) significantly inhibits leukemia progression and effectively reduces primitive FLT3-ITDv AML cells. Moreover, we extend these findings to an AML subtype harboring another tyrosine kinase-activating mutation. In conclusion, our study demonstrates that HDAC8 upregulation is an important mechanism to resist TKIs and promote leukemia maintenance and suggests that combining HDAC8 inhibition with TKI treatment could be a promising strategy to treat FLT3-ITD+ AML and other tyrosine kinase mutation-harboring leukemias.

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