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Validated All-in-One™ qPCR Primer for FOXO1(NM_002015.3) Search again
Product ID:
HQP005747
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
FKH1, FKHR, FOXO1A
Gene Description:
forkhead box O1
Target Gene Accession:
NM_002015.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene belongs to the forkhead family of transcription factors which are characterized by a distinct forkhead domain. The specific function of this gene has not yet been determined; however, it may play a role in myogenic growth and differentiation.
Gene References into function
- fuses with pax3 protein and affects the transcriptional regulation of IGF-I receptor
- cooperation with C-EBP beta in differentiating human endometrial stromal cells
- PAX3-FKHR and PAX7-FKHR gene fusions are prognostic indicators in alveolar rhabdomyosarcoma.
- Transcriptional repression of D-type cyclins (in Class III transcripts)is required for FKHR mediated inhibition of cell cycle progression and transformation.
- Pax3-FKHR allele causes lethal developmental defects in knock-in mice but might be insufficient to cause muscle tumors
- a new mechanism for androgen-mediated prostate cancer cell survival and establish FKHR as nuclear target for both AKT-dependent and -independent survival signals in prostate cancer cells.
- FKHR and HOXA10 interact directly and can function cooperatively to stimulate IGFBP-1 promoter activity in endometrial cells
- Hepatocyte nuclear factor-4 is a novel downstream target of insulin via this protein, which acts a a signal-regulated transcriptional inhibitor.
- results identify a novel signaling pathway linking estrogen action to Pak1 signaling, and Pak1 to FKHR, suggesting that Pak1 is an important mediator of estrogen's cell survival functions
- results indicate that signaling via protein kinase B to forkhead transcription factor FKHR can account for the effect of insulin to regulate peroxisome proliferator-activated receptor-gamma coactivator-1 promoter activity via the insulin response sequenc
- Constitutive phosphorylation of FKHR transcription factor is associated with acute myeloid leukemia
- fMLP-stimulated neutrophils coordinate the regulation of FOXO transcription factors and the survival factor Mcl-1, a mechanism that may allow neutrophils to alter their survival.
- Analysis of amino acids that contribute to the nuclear/cytoplasmic shuttling of FOXO1 protein.
- androgens induce increased activity of an acidic cysteine protease, which in turn cleaves FKHR, a mechanism by which androgens protect prostate cancer cells from the killing effect of FKHR.
- FOXO factors are important for glucocorticoid-stimulated hPDK4 expression
- FOX01 induces atrophy-related uibiquiitin ligase and causes akeletal muscle atrophy.
- A fusion of FOXO1A and PAX3 proteins was used in the diagnosis of a solid alveolar rhabdomyosarcoma.
- in the RD embryonal rhabdomyosarcoma cell line, PAX3-FKHR upregulates expression of the gene encoding the chemokine receptor CXCR4
- data suggest that phosphorylation-dependent degradation of FoxO1 by means of proteasomes plays a role in oncogenic transformation by P3k and Akt
- Chromatin immunoprecipitation results demonstrate in vivo the association of human FOXO1 with the cyclin D2 promoter in untreated rat granulossa cells and release of FOXO1 from the cyclin D2 promoter upon addition of FSH plus activin.
- TNF induces activation of the FOXO1 transcription factor, which acts as a master switch to control apoptosis
- Pax3/FKHR regulates a distinct but overlapping set of genes relative to Pax3 in tumor cells and the global set of Pax3 and Pax3/FKHR gene targets is cell-type specific.
- PAX3, PAX7 and their fusions with FKHR are each expressed in rhabdomyosarcoma tumors as a consistent mixture of functionally distinct isoforms
- FHL2 inhibits FOXO1 activity in prostate cancer cells by promoting the deacetylation of FOXO1 by SIRT1
- persistent activation of PI3K results in Akt-dependent sequestration of FoxO1 outside the nucleus of T cells interacting with APCs; this compartmentalization process can affect T cell growth after Ag recognition
- The carboxyl-terminal region lysines of Foxo1 is acetylated by p300 and stimulates Foxo1-induced transcription of IGF-binding protein-1.
- FOXO1A regulation of the IGFBP1 expression is cell type-dependent
- Acetylation, catalyzed by CREB-binding protein, regulates the function of Foxo1 through altering the affinity with the target DNA and the sensitivity for phosphorylation.
- Data show that Foxo1 and Foxo3a are the most abundant Foxo isoforms in mature endothelial cells and that overexpression of constitutively active Foxo1 or Foxo3a, but not Foxo4, significantly inhibits endothelial cell migration and tube formation in vitro
- Differentiating HESCs become dependent on progesterone signaling for survival through induction and reversible inactivation of FOXO1 suggesting a novel mechanism that links decidualization of the endometrium to menstruation
- These studies show IGF-I phosphorylation of FKHR and FKHRL1 via a PI3-K-dependent pathway in neuroblastoma cells.
- FOXO1A acts as a selective tumor suppressor in alveolar rhabdomyosarcoma.
- PGC-1alpha gene expression is down-regulated by Akt- mediated phosphorylation and nuclear exclusion of FoxO1 in insulin-stimulated skeletal muscle
- Foxo1 is involved in the nucleocytoplasmic translocation of PDX-1 by oxidative stress and the JNK pathway
- The mutant FoxO1 transgene prevents pancreatic beta cell replication in 2 mouse models of beta cell hyperplasia
- FoxO proteins promote hepatic glucose production through multiple mechanisms and contribute to the regulation of other metabolic pathways important in the adaptation to fasting and feeding in the liver
- FOXO1A variation is rare and is unlikely to contribute to type 2 diabetes in either Caucasian or African-American populations
- C5b-9 regulation of the cell cycle activation in aortic endothelial cells through Akt pathway is dependent on inactivation of FOXO1
- versatile nature of FOXO1A in the regulation of a number of decidualization-specific genes
- Differential expression of FOXO1 and FOXO3a confers resistance to oxidative cell death upon endometrial decidualization.
- Expression of FOXO1A inhibited, and its knockdown promoted, cell proliferation or survival in prostate cancer. FOXO1A inhibited androgen- and androgen receptor-mediated gene regulation and cell proliferation.
- FOXO1 and SREBP-1c have roles in insulin regulation of cholesterol 7alpha-hydroxylase expression
- We demonstrate, for the first time in human skeletal muscle, that the regulation of Akt and its downstream signalling pathways GSK-3beta, mTOR and Foxo1 are associated with both the skeletal muscle hypertrophy and atrophy processes.
- Expression of the EBV genes for latent membrane protein 1 and latent membrane protein 2A decreases FoxO1 expression.[FOXO1]
- We show here that EGCG induces phosphorylation of insulin-sensitive residues on the transcription factor FOXO1a.
- PAX3-FKHR fusion protein plays a critical role in the pathogenesis of alveolar rhabdomyosarcomas by influencing the commitment and differentiation of the myogenic cell lineage.
- these data implicate specific members of the FOX family of TFs (FOXC1, C2, P1, P4, and O1A) not previously suggested in heart failure pathogenesis.
- PAX3-FKHR could induce myogenin expression in undifferentiated myoblasts by a MyoD independent pathway, and that PAX3-FKHR is directly involved in myogenin expression in aRMS cells
- The PI3K/Akt pathway is activated in human hepatoma cells exposed to Cu2+ or Zn2+, resulting in the phosphorylation and subcellular relocalisation of transcription factor FoxO1a.
- Potentially causal mutations in FOXO3A (2/90; 2.2%) and FOXO1A (1/90; 1.1%) were identified in POF patients.
- functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage
- Knockdown of endogenous FOXO1 in human vascular endothelial cells decreases phosphorylation of p70 S6 kinase.
- Insulin-like growth factor 1/insulin signaling activates androgen signaling through direct interactions of Foxo1 with androgen receptor.
- A mechanism involving FoxO1a decreases the activity and expression of hydroxy-methylglutaryl coenzyme A reductase via regulation by fluid shear stress in cultured vascular endothelial cells.
- Foxo-1 and Ang-2/Tie2 are part of the molecular response to shear stress, which may regulate angiogenesis.
- PAX3-FKHR fusion transcripts were positive in 3/7 and PAX 7-FKHR fusion transcripts were positive in 2/7 of alveolar rhabdomyosarcoma patients, respectively, and were all negative in embryonal rhabdomyosarcoma and Control tumors.
- These results indicate that the phosphatidylinositol 3-kinase/Akt/FoxO1 pathway participates in Ang II suppression of hSR-BI/CLA-1 expression and suggests that the endothelial receptor for hSR-BI/CLA-1 is downregulated by the renin-angiotensin system.
- Overexpression of FOXO1A may be the result of PER-453 neuroectodermal tumor line's specific epimutations or imbalances in regulatory factors acting at the promoter and/or 3'-untranslated region.
- FoxO-1 mRNA expression and nuclear protein content were significantly increased in quadriceps of patients with COPD; transcriptional regulation of atrogin-1 and MuRF1 may occur via FoxO-1, but independently of AKT
- In this work we show that PAX3-FKHR, which is a stronger transcriptional activator relative to PAX3, can lead to two apparently irreconcilable outcomes: transformation and terminal myogenic differentiation.
- Expression of phosphorylated FOXO1A is a frequent and early event in gastric tumorigenesis and there is a significant correlation between pFOXO1A and better prognosis.
- developed a pathophysiologically relevant transcriptional profile of PAX3/FKHR and identified a critical target gene for aRMS development
- A protective effect of FOXO1A haplotype on type 2 diabetes development.
- Exerts co-regulatory functions independent of DNA binding; DNA-binding defective form of FOXO1a is transcriptionally active as a co-regulator of progesterone receptor A.
- the proapoptotic role of FKHR is probably regulated by several signaling pathways in prostate cancer
- FOXO1 serves as a tumor suppressor in endometrial cancer cells and is involved in normal growth control and maintenance of genomic stability.
- FOXO1 engages in transcriptional cross talk with progesterone receptor to coordinate cell cycle regulation and differentiation of endometrial stromal cells.
- Significant differences in survival and clinical characteristics between PAX3-FKHR and PAX7-FKHR positive tumors were seen indicating their role in carcinogenesis.
- PAX3-FKHR fusion gene of rhabdomyosarcoma cooperates with loss of p16INK4A to promote bypass of cellular senescence
- FOXO1 transcript levels in RA patients and in SLE patients with active disease activity were significantly lower than those in normal controls, and the FOXO1 transcript levels were inversely correlated with lupus disease activity
- isolated and characterized muscle cells from transgenic mice expressing PAX3-FOXO1 under control of PAX3 promoter. Demonstrate that myoblasts are unable to complete myogenic differentiation because of an inability to up-regulate p57Kip2 transcription
- FOXC1 regulates the expression of FOXO1A and binds to a conserved element in the FOXO1A promoter
- AMPK activated by fluid shear stress is a novel regulator of FoxO1a phosphorylation and protein levels.
- These results suggest that PAX3-FKHR promotes malignant phenotypes such as proliferation, motility, and to suppress differentiation.
- The regulation and function of the forkhead transcription factor, Forkhead box O1, is dependent on the progesterone receptor in endometrial carcinoma.
- O-glycosylation of FoxO1 results in increased expression of a glucose-6-phosphatase reporter gene.
- TXNIP is directly repressed by FOXO1a, modulating the cellular response to oxidative stress and affecting life span
- The FOXO1 gene break-apart FISH probe is a simple and accurate tool to detect the translocations associated with alveolar rhabdomyosarcomas.
- FOXO1 expression and activity are increased in patients with steatohepatitis, and mRNA levels are correlated with hepatic insulin resistance.
- findings define a conserved signaling link between Cdk1 and FOXO1 that may have a key role in diverse biological processes, including the degeneration of postmitotic neurons
- Aberrant activation of CDK1 may contribute to tumorigenesis by promoting cell proliferation and survival via phosphorylation and inhibition of FOXO1.
- GlcNAcylation of FoxO provides a new mechanism for direct nutrient control of transcription to regulate metabolism and stress response through control of FoxO1 activity
- the transcriptional activity of PAX3/FKHR can be inhibited by the kinase inhibitor PKC412
- MTP is a target of the transcription factor FoxO1 and excessive VLDL production associated with insulin resistance is caused by the inability of insulin to regulate FoxO1 transcriptional activation of MTP [commentary]
- FoxO1 mediates insulin regulation of MTP production and augmented MTP levels may be a causative factor for VLDL overproduction and hypertriglyceridemia in diabetes
- These findings present new insights into the role of the glucocorticoid receptor and FOXO family of transcription factors in the transcriptional regulation of the muscle specific ring finger protein 1 gene
- FOXO1 controls the expression of L-selectin and EDG1 and EDG6, receptors that regulate lymphocyte trafficking
- Dehydroepiandrosterone stimulates phosphorylation of FoxO1 in vascular endothelial cells via phosphatidylinositol 3-kinase- and protein kinase A-dependent signaling pathways to regulate ET-1 synthesis and secretion
- The observation that FoxO-DNA affinity varies between response elements and with posttranslational modifications suggests that modulation of FoxO-DNA affinity is an important component of FoxO regulation in health and misregulation in disease.
- Hepatocyte growth factor inhibits VEGF-FOXO1-dependent gene expression in endothelial cells.
- HNF-4 and Foxo1 are required for reciprocal transcriptional regulation of glucokinase and glucose-6-phosphatase genes in response to fasting and feeding
- COP1 binds FoxO1, enhances its ubiquitination, and promotes its degradation via the ubiquitin-proteasome pathway.
- These data demonstrate that integrin/EGFR cross-talk is required for expression of Egr-1 through a novel regulatory cascade involving the activation of the PI3K/Akt/Forkhead pathway.
- PRMT1 methylates FOXO1 at conserved Arg248 and Arg250 within a consensus motif for Akt phosphorylation which directly blocks Akt-mediated phosphorylation of FOXO1.
- Detection of PAX3/7-FKHR fusion gene by one-step RT-PCR is useful in the diagnosis of rhabdomyosarcomas (RMS) and that AChR-gamma is overexpressed in Chinese RMS patients.
- regulates glucose, lipid and energy metabolism of skeletal muscle. (review)