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Validated All-in-One™ qPCR Primer for FOXO3(NM_201559.2) Search again
Product ID:
HQP061727
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AF6q21, FKHRL1, FKHRL1P2, FOXO2, FOXO3A
Gene Description:
forkhead box O3
Target Gene Accession:
NM_201559.2(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. This gene likely functions as a trigger for apoptosis through expression of genes necessary for cell death. Translocation of this gene with the MLL gene is associated with secondary acute leukemia.
Gene References into function
- Control of cell cycle exit and entry by protein kinase B-regulated forkhead transcription factors
- FKHRL1 role in downregulation of HMG-CoA synthase
- TRAIL is a direct target of FKHRL1
- these results indicate that the proteolytic cleavage of FOXO3a by caspases may represent a novel regulatory mechanism of FOXO3a activity during death receptor signaling.
- 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.
- up-regulation of FoxO3a by paclitaxel can result in increased levels of Bim mRNA and protein, which can be a direct cause of apoptosis in breast cancer cells
- FOXO3a is a downstream target of Akt in endothelial cells that can promote apoptosis via FLIP down-regulation and activation of the extrinsic apoptotic pathway
- sterol carrier protein 2 is upregulated by the daf-16-like Forkhead transcription factor FOXO3a
- FoxO3a controls expression of BTG1 and subsequent regulation of protein arginine methyl transferase activity.
- FOXO3a is a barrier to hematopoietic transformation that is overcome by phosphorylation and cytoplasmic relocalization induced by the expression of NPM-ALK.
- FLT3 can negatively regulate Foxo transcription factors, thereby promoting cell survival and proliferation.
- FOXO factors are important for glucocorticoid-stimulated hPDK4 expression.
- Results describe the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid-differentiated human SH-SY5Y neuroblastoma cells.
- MUC1 regulates the FOXO3a signaling pathway in a survival response to oxidative stress.
- conditional activation of FoxO3a leads to accumulation of BCL6 and down-regulation of cyclin D2 at protein and mRNA levels
- the activation of FKHRL1 seems to be recognized as one of the specific features of invasive ductal carcinoma of the breast.
- Vpr interferes with the suppressive effects of insulin on FOXO-mediated transcription of target genes via 14-3-3.
- Balloon angioplasty leads to the phosphorylation of FKHRL1 and decreased expression of p27, thereby promoting a proliferative phenotype in vascular smooth muscle
- FOXO3a, is involved in the transcriptional activation of prosurvival and proapoptotic molecules in tumor cells.
- conditional activation of FoxO3a leads to induction of Bim expression and apoptosis
- FOXO3a expression and reduced p27KIP1 promoter transactivation are seen in the progression of LNCaP human prostate cancer cells to androgen independence
- Induction of androgen receptor expression by P13K/Akt downstream substrate, FOXO3A, and their role in apoptosis of LNCAP prostate cancer cells is presented.
- 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
- These studies show IGF-I phosphorylation of FKHR and FKHRL1 via a PI3-K-dependent pathway in neuroblastoma cells.
- RUNX3 cooperates with FoxO3a/FKHRL1 to participate in the induction of apoptosis by activating Bim
- FKHRL1 regulates the human inducible nitric-oxide synthase promoter via a specific enhancer sequence.
- Glucocorticoid receptor-mediated FOXO3a inactivation is an important mechanism contributing to glucocorticoid-mediated mammary epithelial cell survival.
- Differential expression of FOXO1 and FOXO3a confers resistance to oxidative cell death upon endometrial decidualization.
- FoxM1 and FoxO3a cooperate to regulate ERalpha gene transcription
- We conclude that Noxa and Bim establish a connection between FKHRL1 and mitochondria, and that both BH3-only proteins are critically involved in FKHRL1-induced apoptosis in neuroblastoma.
- Potentially causal mutations in FOXO3A (2/90; 2.2%) and FOXO1A (1/90; 1.1%) were identified in POF patients.
- FKHRL1 is associated with the apoptosis-inducing effect of endogenous nitric oxide suppression in cancer cells.
- We conclude that knockdown of WTp66ShcA redox function prevents HG-dependent FOXO3a regulation and promotes the survival phenotype.
- the survival of CD4+ central memory T cells depends, at least in part, on the activation and phosphorylation of signal transducer and activator of transcription 5a (STAT5a) and forkhead box O3a (FOXO3a)
- rhFOXO3a is a negative transcription factor of CYR61 in rat VSMC. Suppression of CYR61 is among several mechanisms by which FOXO3a inhibits VSMC proliferation and neointimal hyperplasia.
- ZNF198-FGFR1 activated prosurvival signaling pathways, resulting in elevated phosphorylation of FOXO3a. The phosphorylated residues subsequently sequestered the proapoptotic FOXO3a and BAD to 14-3-3 to prevent apoptosis
- These results provide evidence of direct regulation of Mxi1 by FOXO3a and imply an additional mechanism through which the PI3-kinase/Akt/FOXO pathway can modulate Myc function.
- A critical role of FOXO3a is demonstrated in both spontaneous and homeostatic chemokine-induced survival of chronic lymphocytic leukemia B-cells.
- 3,3'-diindolylmethane -induced cell growth inhibition and apoptosis induction are partly mediated through the regulation of Akt/FOXO3a/GSK-3beta/beta-catenin/AR signaling
- Oxidative stress modulates complement factor H expression in retinal pigmented epithelial cells by acetylation of FOXO3
- regulation of FOXO3 by AMPK may play a crucial role in fine tuning gene expression programs that control energy balance and stress resistance in cells throughout life
- Akt blocks MstI-triggered FOXO3 nuclear translocation by phosphorylating MstI, promoting cell survival.
- FKHRL1 antagonized deregulates proliferation and induced apoptosis in myelogenous leukemia-derived cell lines.
- Study demonstrates that the methyl groups of specific thymine bases within the consensus sequence are important for FOXO3a-DNA-binding domain recognition of the consensus binding site.
- Despite potential for FOXO3 haploinsufficiency to cause ovarian failure, FOXO3 mutations or common SNPs are not common cause of either premature ovarian failure or primary amenorrhea.
- Suggest new pathway for the induction of oxidative stress by AGEs involving FKHRL1 inactivation and MnSOD suppression via Ser-36 phosphorylation of p66(shc) in human kidney cells.
- forkhead box O3 (FOXO3a) promotes apoptosis of endothelial cells through activation of c-Jun N-terminal kinase (JNK) and suppression of NF-kappaB
- activation of PKCtheta inhibits the FOXO3a/ERalpha/p27(Kip1) axis that normally maintains an epithelial cell phenotype and induces c-Rel target genes, thereby promoting proliferation, survival, and more invasive breast cancer.
- FKHRL1 siRNA underwent rapid apoptosis after erythropoietin (EPO) deprivation in the UT-7/EPO cells
- FOXO3a (forkhead box O3) increased the expression of MMP-3 (stromelysin-1) but decreased the expression of tissue inhibitors of metalloproteinases-1 (TIMP-1)in human umbilical vein endothelial cells
- FOXO3a plays an important role in HIV-1-induced cell death of human macrophage.
- FOXO3 mutation did not show any pathogenic change in lymphedema patients
- FOXO3A mediates peroxiredoxin III expression, and this may play a critical role in the resistance to oxidative stress in cardiac fibroblasts
- There is a novel pathway in cell growth and tumorigenesis through negative regulation of FOXO3a by RAS-ERK and MDM2.
- Inactivation of FOXO3a after GR activation is an important mechanism contributing to GC-mediated repression of uPA gene expression in breast epithelial and cancer cells.
- The role of FOXO3a in the immunological control of HIV disease progression is reported.
- Functional interaction between FOXO3a and ER plays a critical role in suppressing estrogen-dependent breast cancer cell growth and tumorigenesis in vivo. This suggests that agents that activate FOXO3a may
- Data show that FOXO3a interacts with ATM to promote phosphorylation of ATM at Ser 1981 and prompting its downstream mediators to form nuclear foci in response to DNA damage.
- Akt/FOXO3a signaling is an important regulator of endothelial progenitor cells maturation
- positive correlation between Foxo3a and p27(kip1)expression in non-Hodgkin's lymphomas
- These results identify p66Shc and FOXO3a as novel partners of beta(1)Pix and represent the first direct evidence of beta(1)Pix in cell proliferation via Erk/p66Shc-dependent and Akt-independent mechanisms.
- FOXO3a mediates the androgen-dependent regulation of FLIP and contributes to TRAIL-induced apoptosis of LNCaP cells.
- The inhibition of FOXO3a-mediated activation of the p27 gene by the high aberrant expression of c-Myc in many tumor cells likely contributes to their uncontrolled proliferation and invasive phenotype.
- Akt and its downstream targets FoxO3a and GSK3 regulate a survival pathway in VSMCs and that their deregulation due to a reduction of IGF1R signaling may promote apoptosis in atherosclerosis.
- SGK1 negatively regulates the pro-apoptotic transcription factor Forkhead box O3a (FoxO3a) via phosphorylation and exclusion from the nucleus.
- LMP1 triggers the PI3K/Akt pathway to inactivate FOXO3a and decrease DDB1, which can lead to repression of DNA repair and may contribute to genomic instability in human epithelial cells
- Nuclear accumulation of Foxo3a in tumor cells was correlated with increased radiosensitivity and with improved patient survival.
- LPS and bacterial infection inactivate Foxo3a in intestinal epithelia via the PI3K pathway and inactivated Foxo3a leads to the upregulation of IL-8 by suppressing inhibitory IkappaBalpha.
- FOXO3a acetylation is a late event response of CML progenitors to imatinib eventually contributing to the development of a drug-resistant phenotype through mechanisms promoting re-phosphorylation and transcriptional attenuation of FOXO3a.
- isoflavone-induced inhibition of cell proliferation and induction of apoptosis are partly mediated through the regulation of the Akt/FOXO3a/GSK-3beta/AR signaling network.
- intracellular localization of the FOXO family member FOXO3a
- cellular signalling events both up- and down-stream of FOXO3a are critical to the generation and the maintenance of lymphocyte memory
- Foxo3a could negatively regulate myocardin expression levels through up-regulating catalase and the consequent reduction of ROS levels
- Data propose that SIRT3 and FOXO3a comprise a potential mitochondrial signaling cascade response pathway.
- analysis of the intramolecular interaction in FOXO3a and its binding with p53
- Scleroderma serum-induced EPC apoptosis is mediated chiefly by the Akt-FOXO3a-Bim pathway, which may account, at least in part, for the decreased circulating EPC levels in scleroderma patients.
- FOXO3a plays a critical role in the apoptosis and G0 arrest phase of human immunodeficiency virus 1-infected CD4-positive T lymphocytes.
- Low expression of Foxo3a is associated with ovarian cancer.
- expression of miR-182 increases with progression from primary to metastatic melanoma and inversely correlates with FOXO3 and microphthalmia-associated transcription factor levels