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Validated All-in-One™ qPCR Primer for RUNX2(NM_001024630.3) Search again
Product ID:
HQP114766
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AML3, CBF-alpha-1, CBFA1, CCD, CCD1, CLCD, OSF-2, OSF2, PEA2aA, PEBP2aA
Gene Description:
RUNX family transcription factor 2
Target Gene Accession:
NM_001024630.3(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 is a member of the RUNX family of transcription factors and encodes a nuclear protein with an Runt DNA-binding domain. This protein is essential for osteoblastic differentiation and skeletal morphogenesis and acts as a scaffold for nucleic acids and regulatory factors involved in skeletal gene expression. The protein can bind DNA both as a monomer or, with more affinity, as a subunit of a heterodimeric complex. Mutations in this gene have been associated with the bone development disorder cleidocranial dysplasia (CCD). Transcript variants that encode different protein isoforms result from the use of alternate promoters as well as alternate splicing. [provided by RefSeq].
Gene References into function
- clavicular dysplasia was more pronounced with the R19OW mutation, while the bone density was markedly reduced in individuals with either R19OW or deletion of nucleotide C821
- Analysis of the three-dimensional structure of the DNA binding runt domain of the RUNX2 protein and its interaction with DNA provide insight into how missense mutations affect RUNX2 function and cause cleidocranial dysplasia.
- RT-PCR analysis of human bone marrow stromal cells during osteogenesis in vitro: the mRNA levels of bone morphogenetic protein-2 (BMP-2), bone sialoprotein-II (BSP), osteopontin (OP) and cbfa-1 increased with culture time in osteogenic medium.
- is an essential transcription factor for the regulation of osteoblast differentiation
- regulatory signals are active at transcriptional subnuclear sites
- Runx2 expression in osteoblasts is reduced by hypoxia, and may be a mechanism of osteoporosis by decreased vascular supply.
- Differential regulation of Cbfa1/Runx2 and osteocalcin gene expression by vitamin-D3, dexamethasone, and local growth factors in primary human osteoblasts
- variants may be related to genetic effects on bone mineral density and osteoporosis
- Cleidocranial dysplasia could result from much smaller losses in the RUNX2 function than has been envisioned on the basis of the conventional haploinsufficiency model.
- RUNX2 is negatively regulated by the phosphorylation of two conserved serines
- TWIST inactivation reduces expression and DNA binding to the osteocalcin promoter in osteoblasts.
- This protein is regulated by human basic fibroblast growth factor.
- Cbfa1 is required in mediating the bone anabolic effects of parathyroid hormone.
- Runx2/Cbfa1 activity increases through a posttranslational mechanism involving phosphorylation of key residues and has a role in osteoblastic differentiation
- Cbfa1 is a key regulatory factor in the vascular calcification observed in dialysis patients and is up-regulated in response to many uremic toxins.
- Telomerase accelerates osteogenesis of bone marrow stromal stem cells by upregulation of CBFA1, osterix, and osteocalcin.
- Cleidocranial dysplasia (CCD) is an inherited autosomal-dominant skeletal disease caused by heterozygous mutations in the RUNX2 protein.
- Expression of Runx2 in prostate cancer may be the molecular switch that is associated with expression of various bone-specific factors in prostate cancer.
- Runx2 is ectopically expressed in breast cancer cells and that one isoform of Runx2 can activate bsp expression in these cells.
- six novel mutations causing 2 amino acid substitutions and four frameshift mutations were identified in the RUNX2 gene of Italian cleidocranial dysplasia patients.
- Runx2 has a role in parathyroid hormone-induced anti-apoptotic signaling in osteoblasts, which is shortened by proteasomal degradation
- mechanical stress plays a key role in the progression of OPLL through an increase in Cbfa1 expression
- The regulation of SOST expression by Cbfa1 suggests a potential role for the sclerosteosis gene in homeostatic regulation of osteoblast differentiation and function.
- RUNX1 and RUNX2 regulate TIMP1 gene expression
- Runx2 has a role in menin-induced bone morphogenetic protein 2- and transforming growth factor beta-regulated osteoblastic differentiation
- Runx2 expression in breast cancer cells provides a molecular phenotype that enables the interactions between tumor cells and the bone microenvironment that lead to osteolytic disease.
- As a target gene of endostatin, cbfa1/osf2 was found to be specifically expressed in granulocytes in human breast neoplasms.
- RUNX2 DNA binding is regulated by IGF-1 through sequential activation of the PI3K/Pak1 and ERK1/2 signaling cascade
- Osteocalcin mRNA was down-regulated in Apert osteoblasts carrying the FGFR2 P253R mutation, Runt-related transcription factor-2 (RUNX2) mRNA was differentially spliced, and FGF2 secretion was greater.
- Growth hormone attenuates the transcriptional activity of Runx2 by facilitating its physical association with Stat3beta
- Physiologic coupling of osteoblast differentiation to cell cycle withdrawal is mediated through runx2 and p27KIP1, and these processes are disrupted in osteosarcoma.
- PLZF plays important roles in early osteoblastic differentiation as an upstream regulator of CBFA1
- Fidelity of Runx2 intranuclear organization is necessary for expression of target genes that mediate the osteolytic activity of metastatic breast cancer cells.
- Capability of Imatinib to induce an anti-leukemic effect in Core Binding Factor (CBF)-leukemia patients.
- 4 new genes may be under the control of Cbfa1; 3 of them, SelM, elF-4AI, & RPS24, seemed to be linked to a global change in cellular metabolism & cell growth; the CD99/MIC2 gene was strongly overexpressed in cells presenting high levels of Deltacbfa1
- Runx2 collaborates with Oct-1 and contributes to the expression of a mammary gland-specific gene.
- RUNX2/CBFA1 has a critical role in the decreased bone formation in multiple myeloma
- We propose that nuclear-cytoplasmic shuttling of RUNX2 may modulate its transcriptional activity, as well as its ability to interface with signal transduction pathways that are integrated at RUNX2 containing subnuclear sites.
- Runx2-regulated MMP9 levels are functionally related to the invasion properties of cancer cells
- Runx2 has a role in organizing gene transcription in developing and maturing osteoblasts [review]
- The results of the present research contribute to the deeper understanding of the genetic architecture of femoral size and introduce the issues of site and sex dependency of the extent of RUNX2 effect.
- silencing Runx2 with siRNA in myeloma cells suppressed OPN mRNA and protein expression, critical for the proangiogenic effect of myeloma cells
- RUNX factors participate in prostate epithelial cell function and cooperate with an Ets transcription factor to regulate PSA gene expression
- A novel RUNX2 missense mutation has been found in members of a family clinically diagnosed with cleidocranial dysplasia.
- The cleidocranial dysplasia phenotype can be caused by a splice site mutation, which results in the deletion of N-terminus amino acids containing the QA stretch in RUNX2 that contains a previously unidentified second nuclear localization signal.
- Smad6 interacts with Runx2 and mediates Smad ubiquitin regulatory factor 1-induced Runx2 degradation
- RUNX2 phosphorylation by cdc2 may facilitate cell cycle progression possibly through regulation of G(2) and M phases, thus promoting endothelial cell proliferation required for tumor angiogenesis
- Of 16 SNPs in RUNX2 and its two promoters (P1 and P2), only SNPs in the P2 promoter were significantly associated with bone density.
- Regulation of Gsalpha protein by Runx2 seems to be of particular interest considering the increasing evidences on bone metabolism regulation by G proteins
- A severe calvarial phenotype is described that is associated with novel mutations in the C-terminal region of RUNX2 distal to the DNA-binding runt domain.
- In dental follicle cells, gene expression of runx2, DLX-5, and MSX-2 was unaffected during osteogenic differentiation in vitro.
- An unexpected interaction is found between transgenic Runx2 and mouse parathyroid hormone-related protein (PTHrP) in controlling the rate of chondrocyte proliferation.
- autocrine BMP production is necessary for the RUNX2 transcription factor to be active and that BMPs and RUNX2 cooperatively interact to stimulate osteoblast gene expression.
- BMP-2 stimulates Runx2 acetylation
- The transcription axis of Cbfa-1 (Runx-2) is crucial in maintaining equilibrium of bone formation and resorption. Heparin affects expression in osteoblast culture.
- Runx2 directly binds to the osteoblast specific binding elements 2 elements and transactivates the human NELL-1 promoter.
- Results show that RUNX2 is hyper-phosphorylated by CDK1/cyclin B during mitosis in osteoblastic cells.
- Runx2 is a critical mechanistic link between cell fate, proliferation and growth control
- F promoter of ERalpha activity may be tightly regulated by a dynamic interplay between these two Runx2 sites, with a predominance of negative effect of the Runx2 (a) site.
- Cbfa1 may act as a repressor of early stem cell markers such as human TERT as one possible mechanism for facilitating cellular differentiation.
- Runx2 protein is stable during cell division and is bound to chromosomes during mitosis through sequence-specific DNA binding and thus has an active role in retaining phenotype during cell division to support control of gene expression in progeny cells.
- Cbfb enhances osteogenic differentiation of mesenchymal stem cells by stabilizing Cbfa-1 proteins.
- findings demonstrate that Runx2 expression is active in variable chondrosarcomas compared to enchondromas, suggesting its importance in growth and differentiation of neoplastic cartilage
- Thus, our results suggest that Cbfalpha1 upregulates DMP1 gene expression differentially that may contribute to the spatial-temporal expression pattern of DMP1 during odontoblast differentiation.
- the RUNX2 and YAP65 interaction has a novel role in oncogenic transformation that may be mediated by modulation of p21(CIP1) protein expression
- In this study of a 14-yr-old boy with typical cleidocranial dysplasia phenotype, the authors found a novel CBFA1/RUNX2 gene mutation.
- STAT3, Runx2, and steroid receptor coactivator-1 are critical molecules in mediating leptin-stimulated cell osteogenesis in TOLF (thoracic ossification of ligament flavum)
- The results highlight the importance of the RUNX2 promoter 2 polymorphism in femur neck bone density determination.
- Runx2 and HDAC3 repress BSP gene expression and that this repression is suspended upon osteoblastic cell differentiation.
- A novel missense mutation in the RUNT-domain (P210S) of RUNX2 was identified in 3 Japanese cleidocranial dysplasia siblings; they showed a wide variation in the number and position of supernumerary teeth
- Runx2 regulates bone development, bone maturation, and bone maintenance through the regulation of osteoblast differentiation and function [review]
- Histone deacetylase 7 associates with Runx2 and represses its activity during osteoblast maturation in a deacetylation-independent manner
- Runx2 phosphorylation results from addition of hNELL1 protein
- novel mutation of RUNX2 disrupts the protein-DNA interaction
- TFIIA gamma together with ATF4 and Runx2 stimulates osteocalcin promoter activity and endogenous mRNA expression.
- Runx2-mediated activation of the Bax gene increases osteosarcoma cell sensitivity to apoptosis
- RUNX2 influences joint formation by affecting the differentiation pathways of chondrocytes and osteoblasts.
- angiopoietin-1 is downstream of Runx2 in both OPLL primary cells and osteoblasts. Angiopoietin-1 may play an important role in ectopic ossification.
- In cotransfection experiments with an osteocalcin (OC) promoter construct, we confirmed that only RUNX2wt and RUNX2Delta7 could upregulate the OC promoter activity in the osteosarcoma cell line.
- RUNX2 appears to influence risk of CL/P through a parent-of-origin effect with excess maternal transmission
- Polymorphisms in the RUNX2 promoter is significantly associated with the hand bone length and bone mineral density.
- Cbfa-1 may play a role in calcification processes in human thyroid papillary carcinoma tissues.
- These data suggest a functional contribution of Runx-2-regulated galectin-3 expression to glial tumor malignancy.
- the region between -3 kb and -1 kb is required for the minimal skeletal tissue-specific expression of Runx2, and that the region between -155 bp and -75 bp is important for its basal transcription, which may be in part mediated by HIF2A in bone tissues.
- This is the first report demonstrating significant upregulation in expression of Runx2 and Osterix by TGF-beta3 induction of human adipose-derived stromal cells during in vitro chondrogenesis.
- Dats suggest that sparse neovascularization into areas underlying the atherosclerotic plaques' necrotic cores, where Cbfa1-expressing cells reside, might explain the rarity of ectopic bone formation in the arterial wall.
- FHL2-beta-catenin interaction potentiates beta-catenin nuclear translocation and TCF/LEF transcription, resulting in increased Runx2 and alkaline phosphatase expression, which was inhibited by the Wnt inhibitor DKK1.
- These data on a variant of RUNX2 suggest that lipid metabolism might be affected by genetic polymorphisms in the promoter region.
- the RUNX2 gene was analyzed within a CCD family from China, and a novel missense mutation (c. 475G --> C [p.G159R]) was identified.
- E4BP4 has a role as osteoblast transcriptional repressor in inhibiting both Runx2 and Osterix in myeloma bone disease
- A novel role of Runx2 in up-regulating the vicious cycle of metastatic bone disease, in addition to Runx2 regulation of genes related to progression of tumor metastasis.
- Hey1 and Runx2 were shown to act synergistically in BMP9-induced osteogenic differentiation, and Runx2 expression significantly decreased in the absence of Hey1, suggesting that Runx2 may function downstream of Hey1
- This study identifies RUNX2 as a target for heavy metal-induced osteotoxicity.
- the HY(hypertrophy) box is the core element responsive to RUNX-2 in human COL10A1 promoter