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- Table of Contents
1 Citations 5 Q&As
Facts about Forkhead box protein O3.
Participates in post-transcriptional regulation of MYC: after phosphorylation by MAPKAPK5, promotes induction of miR-34b and miR-34c expression, two post-transcriptional labs of MYC that bind to the 3'UTR of MYC transcript and prevent its interpretation (PubMed:21329882). In response to metabolic stress, translocates to the mitochondria where it promotes mtDNA transcription (PubMed:23283301).
Human | |
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Gene Name: | FOXO3 |
Uniprot: | O43524 |
Entrez: | 2309 |
Belongs to: |
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No superfamily |
AF6q21 protein; AF6q21; DKFZp781A0677; FKHRL1; FKHRL1MGC31925; FKHRL1P2; forkhead box O3; forkhead box protein O3; forkhead homolog (rhabdomyosarcoma) like 1; Forkhead in rhabdomyosarcoma-like 1; forkhead, Drosophila, homolog of, in rhabdomyosarcoma-like 1; FOXO2; FoxO3; FOXO3A; FOXO3Aforkhead box O3A; MGC12739
Mass (kDA):
71.277 kDA
Human | |
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Location: | 6q21 |
Sequence: | 6; NC_000006.12 (108559825..108684774) |
Ubiquitous.
Cytoplasm, cytosol. Nucleus. Mitochondrion matrix. Mitochondrion outer membrane; Peripheral membrane protein; Cytoplasmic side. Retention in the cytoplasm contributes to its inactivation (PubMed:10102273, PubMed:15084260, PubMed:16751106). Translocates to the nucleus upon oxidative stress and in the absence of survival factors (PubMed:10102273, PubMed:16751106). Translocates from the cytosol to the nucleus following dephosphorylation in response to autophagy-inducing stimuli (By similarity). Translocates in a AMPK-dependent manner into the mitochondrion in response to metabolic stress (PubMed:
The FOXO3 marker is a highly relevant gene for a wide variety of applications. It interacts with several proteins, including YWHAB/14-3-3-beta, CAMK2A, and calcineurin A. The gene is present in most human tissues, but it is rarely detected in cells of other species. Boster scientists are eligible to submit their findings for product credits.
The FOXO3 gene is an important master regulator of aging. The use of the FOXO3 SNP rs2802292 to determine if a person responds to conventional therapies has potential. In addition, it may facilitate novel research directions by allowing researchers to understand how SNPs modulate cellular processes. Moreover, understanding how SNPs affect gene function may shed light on associated phenotypes.
As a key mediator of biological processes, FOXO3 regulates genes that promote autophagy in cancer cells and induces cell death under persistent stress conditions. It has also been recognized as a tumor suppressor in human breast cancer and its levels correlate with poor patient survival. Its role is crucial in the fight against cancer and is important in the prevention of aging-related diseases. The FOXO3 marker is widely used in cancer research because of its numerous potential uses.
The FOXO3 gene is regulated by a cytokine called SNHG5 which binds to the FOXO3 protein. Its ubiquitination is inhibited by USP21 and promotes autophagy. Both SNHG5 and FOXO3 have important roles in regulating thyroid cancer. Moreover, FOXO3 is associated with autophagy, which is a significant factor in the progression of thyroid cancer.
The FOXO3 marker is validated by Boster Bio using different platforms. The antibody reacts to both Human, Mouse, and Rat cells. As a result, it is specific and high affinity. Furthermore, Boster Bio awards product credit to the first reviewer. This incentive is available to all scientists world-wide. So, why wait any longer? Invest in the FOXO3 marker and discover new applications for it.
Besides its prognostic value, the FOXO3a gene has potential for research. It has been associated with poor prognosis in triple-negative breast cancer, hepatocellular carcinoma, and glioma. However, it is difficult to validate FOXO3a's utility in large cancer cohorts. Therefore, large-scale studies in patient populations are needed to confirm the FOXO3 marker's utility.
The FOXO3 gene is a tumor suppressor in animals. Its overexpression in cancer patients may contribute to drug resistance. Furthermore, a phosphorylated FOXO3a gene inhibits nuclear import and export. As a result, the overexpression of FOXO3a in cancer cells leads to the development of various diseases. For these reasons, it is essential to understand the role of FOXO3 gene in cancer.
Studies have shown that FOXO3 gene polymorphisms have a role in age-related diseases. A recent study revealed that FOXO3 gene polymorphism rs2802292 has an anti-aging effect. Researchers have also shown that rs2802292 has a protective effect on cancer risk in males and females alike. In addition to its benefits for age-related disease, studies have shown that the gene could also predict the risk of nutrient and oxidative stress-related diseases.
FOXO3a has a role in the regulation of ERa gene expression in breast cancer cells. The FOXO3a-ERa complex is a critical regulator of ERa gene expression. Moreover, FOXO3a's expression could be an important factor in the success of endocrine therapy. There is an estrogen-dependent role for FOXO3a in breast cancer. The level of FOXO3a expression in breast cancer cells can affect the effectiveness of chemotherapy.
BAALC is a 180 amino acid protein that interacts with CAMK2A. It is expressed in neural and hematopoietic cells. It is also expressed in most immature blasts from acute leukemia patients. CAMK2A is a member of the kinase family that is activated by Ca2+. BAALC is a potential drug target for CAMK2-related diseases.
NXN-dependent kinase activity was increased in mice expressing the gene. In a Camk2a kinase assay, NXN was detected in mouse brain lysates and from Nestin-NXN-/ mice. Baseline Camk2a activity in control mice and NXN-/ mice was not different. The effects of H2O2 on Camk2a activity were similar in both groups. However, recombinant NXN (rNXN) significantly increased Camk2a activity in the mice lacking Nestin. Moreover, this increased activity in NXN-/ mice was greater than in controls.
CaMKII-NR2B interactions have several other effects, including suppressing inhibitory autophosphorylation of CaMKII and direct generation of sustained Ca2+/calmodulin (CaM)-independent kinase activity. Inhibition of CaM-NR2B interactions may also reduce the downregulation of NMDA receptor activity. Thus, this interaction may be a prototypical mechanism of direct activation by targeting protein-CAMK2A.
NXN is located in cortical dendritic spines, where it colocalizes with CAMK2a. NXN colocalizes with Camk2a at dendritic spines in hippocampus and cortex. They also colocalize with MAP-2. In the same study, NXN and Camk2a were found to co-express in dendritic spines.
The PMCA2 family of proteins contains the human PMCA2b. The hPMCA2b protein has a C-terminal region of 1143-1243 amino acids and a small interaction domain of 539-609 and 511-585 amino acids. The region interacts with calcineurin A and is involved in the negative regulation of the calcineurin-NFAT signaling pathway. In Alzheimer's disease, this protein is implicated as a pathological mediator.
PMID: 9479491 by Anderson M.J., et al. Cloning and characterization of three human forkhead genes that comprise an FKHR-like gene subfamily.
PMID: 9345057 by Hillion J., et al. AF6q21, a novel partner of the MLL gene in t(6;11)(q21;q23), defines a forkhead transcriptional factor subfamily.
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