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Validated All-in-One™ qPCR Primer for RUNX3(NM_004350.2) Search again
Product ID:
HQP021394
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AML2, CBFA3, PEBP2aC
Gene Description:
RUNX family transcription factor 3
Target Gene Accession:
NM_004350.2(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 encodes a member of the runt domain-containing family of transcription factors. A heterodimer of this protein and a beta subunit forms a complex that binds to the core DNA sequence 5'-PYGPYGGT-3' found in a number of enhancers and promoters, and can either activate or suppress transcription. It also interacts with other transcription factors. It functions as a tumor suppressor, and the gene is frequently deleted or transcriptionally silenced in cancer. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- RUNX3 methylation is associated with gastric cancers
- RUNX3/AML-2 binding to the CD11a promoter correlates with increased RUNX3/AML-2 protein levels and enhanced CD11a/CD18 cell surface expression
- These results strongly suggest that RUNX3 is one of the tumor suppressors involved in the pathogenesis of testicular yolk sac tumors in infants.
- results suggest that loss of RUNX3 expression by DNA hypermethylation is frequently associated with the evolution of lung cancer
- Inactivation of RUNX3 gene through allelic loss and promoter hypermethylation might be one of the major mechanisms in hepatocellular carcinogenesis.
- Our results overall suggest that transcriptional inactivation of RUNX3 by promoter hypermethylation may participate in the stomach carcinogenesis.
- Data show that RUNX3 is a target of the acetyltransferase activity of p300 acetyltransferase.
- Transcriptional repression of RUNX3 is caused by promoter hypermethylation of the RUNX3 CpG island in colorectal cancer cell lines.
- Expression of RUNX3 is down regulated in a significant portion of gastric cancer cases; may be involved in gastric carcinogenesis
- RUNX3 regulates RUNX1 expression in human B lymphoid cell lines.
- The percentage of CD4-8+ cells increases and the percentage of CD4+8+ and CD4+8- cells simultaneously decreases in the Runx3-transgenic thymus. Thus, Runx3 can drive thymocytes to select the CD4-8+ lineage.
- an inhibitory element was identified in the KIR2DL4 promoter and an activating element was found in the KIR3DL3 promoter; AML-2 acts as a repressor of expression of both KIR2DL4 and KIR3DL3 in mature NK cells
- Hypermethylation of RUNX3 may play an important role in early events of hepatocarcinogenesis.
- The expression of RUNX3 protein in lung AC might play a pivotal role in tumor progression and patients' survival
- Hypermethylation of p16, RUNX3, and HPP1 in Barreett exophagus may represent independent risk factors for the progression of Barrett esophagus to esophageal cancer.
- RUNX3 aberrant methylation might play an important role in colorectal cancers, especially in poorly-differentiated colorectal cancers.
- findings refute a role for RUNX3 as a tumor-suppressor gene in early-onset gastric carcinogenesis
- RUNX3 is required for the TGF-beta-dependent induction of p21 expression in stomach epithelial cells.
- RUNX3 was found to be inactive in 82% of gastric cancers through either gene silencing or protein mislocalization to the cytoplasm.
- RUNX3 is downregulated by hemizygous deletion at 1p36 in human lung cancer cell lines
- Promoter hypermethylation of RUNX3 gene may occur as an early event in the development of hepatocellular carcinoma (HCC) and that methylation may be a major mechanism for inactivation of RUNX3 gene in HCC.
- Down-Regulation of RUNX3 aberrant methylation is associated with cancer
- RUNX3 gene plays an important role in the pathogenesis of lung cancer, and aberrant methylation is an important mechanism of inactivation of the RUNX3 gene in lung AdC.
- detection of hypermethylation at multiple regions within the RUNX3 CpG island may be useful in the diagnosis and risk assessment of gastric cancer
- RUNX3 cooperates with FoxO3a/FKHRL1 to participate in the induction of apoptosis by activating Bim
- KAP5 gene expression in human hair follicles is regulated by Runx1
- The expression of RUNX3 was studied in esophageal mucosa and squamous cell carcinoma as well as in comparison with clinicopathological profiles.
- analysis of how the RUNX3 gene induces apoptosis in gastric cancer
- results suggest that mammalian RUNX family transcription factors are novel binding partners and substrates for the Pim-1 kinase, which may be able to regulate their activities during normal hematopoiesis as well as in leukemogenesis
- results indicate that although the deregulation of Wnt signalling could contribute to the pathogenesis of a subset of basal cell carcinomas (BCC), RUNX3 appears to be a universal downstream mediator of a constitutively active Shh pathway in BCC
- In breast tumors, hypermethylation of RUNX3 was observed in 23 of 44 cases. Mislocalization of the protein, with or without methylation, seems to account for RUNX3 inactivation in the vast majority of the tumors.
- Runx3 impairs the activity of the proximal regulatory region of the CD36 gene in myeloid cells through in vitro recognition of two functional RUNX-binding elements.
- Methylation rates (MR) in four of the cancer cell lines that lost RUNX3 mRNA ranged from 99.0% to 99.7% (mean, 99.4%), whereas MR in the remaining cell line that expressed RUNX3 mRNA was 0.6%.
- transcription factor Runx3 is induced in T helper type 1 cells in a T-bet-dependent manner, and that both transcription factors T-bet and Runx3 are required for maximal production of interferon-gamma and silencing of the gene encoding IL-4 in Th1 cells
- RUNX3 silencing promotes radioresistance in esophageal cancers
- RUNX3 is involved in TGF-beta-induced expression of p21 and the resulting induction of TGF-beta-dependent G(1) arrest.
- The present data suggest that TGF-beta, LMO1, possibly RUNX3, and GSDM form a regulatory pathway for directing the pit cells to apoptosis.
- Runx3 determines TrkC positive sensory neuron identities through the transcriptional repression of TrkB when Trk-BTrkC double positive neurons differentiate into TrkC single positive neurons.
- Important target of DNA methylation in the evolution of microsatellite instability in gastric cancer.
- A panel of markers including at least RUNX3, CACNA1G, IGF2, and MLH1 can serve as a sensitive and specific marker panel for CIMP(Cpg island methylator phenotype)-high.
- the hypermethylation of RUNX3 gene is a useful biomarker to predict the prognosis in non-small cell lung cancer
- Promoter hypermethylation of RUNX3 is associated with neoplasms
- Eighty-five percent of breast cancer tissues showed downregulated RUNX3 gene expression, whereas it was downregulated in only 25% of normal breast tissues.
- RUNX3 expression suppressed cell proliferation by inducing apoptosis via the death-receptor mitochondria-mediated pathway in human gastric carcinoma MKN-1 cells.
- Results suggest that epigenetic silencing of RUNX3 gene expression by promoter hypermethylation may play an important role in esophageal squamous cell carcinoma development.
- H. pylori infection contributes to Runx3 methylation in gastric cancer tissues...subsequent loss of Runx3 expression may therefore affect gastric carcinogenesis.
- RUNX3 inactivation by promoter hypermethylation and protein mislocalization constitute an early event in breast cancer progression.
- RUNX3 inhibits growth of HCC cells and HCC xenografts in mice in combination with adriamycin
- RUNX3 mRNA expression levels were lower in invasive esophageal squamous cell carcinoma.
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- RUNX was found to be methylated significantly more frequently in NSCLC tissues than noncancerous tissues.
- RUNX3 is a target for repression by EZH2 in gastric cancer cells
- Hypermethylation and LOH appear to be common mechanisms for inactivation of RUNX3 in pancreatic cancer. Therefore, RUNX3 may be an important tumour suppressor gene related to pancreatic cancer.
- shRNAs targeted to gene promoter regions of RUNX3 induced transcriptional repression with chromatin changes characteristic of inaction promoters, which was independent of DNA methylation.
- Downregulation of RUNX3 may play a role in disease progression of esophageal squamous cell carcinoma.
- Findings indicate that RUNX3 inactivation may play an important role in carcinogenesis of the endometrium, especially in high-grade endometrial carcinoma.
- With the increased progression of breast cancer, the expression of RUNX3 protein tends to decrease. The expression of RUNX3 protein has a definite value in judging prognosis in breast cancer.
- RUNX3 methylation carries a 100-fold increase in the risk of bladder tumor. The rate of RUNX3 hypermethylation in primary bladder tumors is 71.2%. This suggests that patterns of promoter methylation are causally associated with bladder tumorigenesis.
- RUNX3 is found to be commonly repressed by the t(8;21) and inv(16) fusion proteins and might have an important role in core-binding factor AML
- Increased Runx3 is associated with ulcerative colitis.
- prevalence of methylation at RUNX3, a polycomb target gene, increased as a function of age at bladder tumor diagnosis and a history of smoking
- genetic variants in RUNX3 may modulate the risk of bladder cancer.
- Data demonstrate that RUNX3 functions as a tumor suppressor by attenuating Wnt signaling.
- Results suggest that RUNX3 has a role in cell proliferation and viability in ovarian cancer.
- Clinical and experimental data support the notion that RUNX3 is a tumor suppressor in human colon cancer.
- RUNX3 could be considered to play an important role in maintaining the chief cell phenotype.
- data suggest RUNX3 inactivation due to promoter hypermethylation in colorectal polyps represents an early event in colorectal cancer (CRC) progression.