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Validated All-in-One™ qPCR Primer for TNFRSF11A(NM_003839.3) Search again
Product ID:
HQP021550
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD265, FEO, LOH18CR1, ODFR, OFE, OPTB7, OSTS, PDB2, RANK, TRANCE-R, TRANCER
Gene Description:
TNF receptor superfamily member 11a
Target Gene Accession:
NM_003839.3(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
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptors can interact with various TRAF family proteins, through which this receptor induces the activation of NF-kappa B and MAPK8/JNK. This receptor and its ligand are important regulators of the interaction between T cells and dendritic cells. This receptor is also an essential mediator for osteoclast and lymph node development. Studies of the mouse counterpart suggest that this receptor directly mediates the osteoprotegerin ligand (OPGL)-induced osteoclastogenesis in osteoclast precursor cells. [provided by RefSeq].
Gene References into function
- Expansile skeletal hyperphosphatasia is caused by a 15-base pair tandem duplication (84dup15) in TNFRSF11A encoding RANK.
- immunohistochemical localization of this protein and its ligand in deciduous teeth
- MIP-1alpha and MIP-1beta induce expression of RANK ligand by stromal cells, thereby stimulating osteoclast differentiation of preosteoclastic cells.
- TAK1-dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB.
- Analysis of a large Spanish kindred confirms that exon 1 contains an insertional mutation in the RANK gene.
- Long-lived immature dendritic cells mediated by TRANCE-RANK interaction
- a tandem duplication in exon 1 of the TNFRSF11A gene may have a role in familial expansile osteolysis
- associated with external apical root resorption
- the 75dup27 mutation causes a Paget's disease of bone-like phenotype
- transforming growth factor-beta promotes osteoclastogenesis in monocytes by stimulation of the p38 mitogen activated protein kinase but continuous exposure abrogates osteoclastogenesis by down-regulation of receptor activator of NF-KB(RANK) expression
- These data suggest that RANK is expressed by monocytes whose activation by RANKL stimulates directed migration involving phosphatidylinositol 3-kinase, phosphodiesterase, and Src kinases.
- RANK is expressed in bone marrow stroma cells & endothelial cells but not myeloma cells. It is involed in IL-6 & IL-11 secretion.
- Review. The RANKL/RANK/OPG system may mediate links between the vascular, skeletal, & immune systems and play a central role in regulating the vascular calcification coincident with declines in skeletal mineralization with age, osteoporosis, or disease.
- disruption of the RANKL-RANK axis with OPG inhibited tumor-induced osteoclastogenesis and decreased bone cancer pain.
- Involvement of RANK/RANKL in dendritic cell-T cell interactions during inflammatory process. RANK expression appears to be limited to sites of immune reaction, both in synovium and in lymph nodes.
- PU.1 regulates RANK gene transcription; this may represent one of the key roles of PU.1 in osteoclast differentiation
- OPG dimer formation is required for the mechanism of inhibition of the RANK-L/RANK receptor interaction
- We review the etiology of inflammatory bone loss, the RANK/RANK-ligand/OPG pathway, and the clinical development of anti-RANK-ligand therapy.
- By upregulating IL-8, the RANKL/RANK system may contribute to the pathogenesis of B chronic lymphocytic leukemia.
- a functional RANK expressed on osteosarcoma cells
- Expression of RANK-Fc by genetically modified Mesenchymal stem cells may be a feasible option for the prevention of bone loss induced by ovariectomy.
- results suggest that +34863G > A and +35928insdelC polymorphisms in RANK are possible genetic factors for low Bone mineral density in postmenopausal women
- This review describes the most recent knowledge on the OPG-receptor activator of nuclear factor-kappaB (RANK)-RANK ligand (RANKL) triad and its involvement in bone oncology.
- Although the mutation in the Iranian and four of the previously described FEO pedigrees was the same, haplotypes based on the intragenic SNPs suggest that the mutations do not share a common descent.
- A major haplotype in block 5 of Tumor Necrosis Factor receptor superfamily member 11a (RANK) was significantly associated with higher stature in Caucasians.
- Review highlights the receptor activator of nuclear factor-kappa B ligand (RANKL)/RANK/osteoprotegerin (OPG) system and its role in the regulation of bone resorption.
- RANK contributes to osteoclastic bone resoption in RA patients.
- RANK/RANKL/OPG system mediates the effects of calciotropic hormones and, consequently, alterations in their ratio are key in the development of several clinical conditions--REVIEW
- The OPG/RANKL/RANK system constitutes the important element of controlling the number of active osteoclasts by the osteoblasts.
- cDNA microarray and quantitative RT-PCR analyses demonstrate that RANK-positive osteosarcoma cells are the target of RANKL as well as osteoclasts/osteoclast precursors.
- RANK is expressed on prostate cancer cells and promotes invasion in a RANKL-dependent manner
- differences in the RANK, RANKL, and OPG expression in odontogenic epithelial tumors...could contribute to the differential bone/tooth resorption activity in these lesions
- The relative protection against bone erosions in spondylarthritis cannot be explained by qualitative or quantitative differences in the synovial expression of RANKL, OPG, and RANK.
- Data reveals for the first time that OPG/RANK/RANKL are expressed in the pathological thyroid gland by follicular cells, by malignant parafollicular cells as well as in metastatic lymph node microenvironment.
- Osteoclast-poor osteopetrosis with agammaglobulinemia due to TNFRSF11A (RANK) mutation is reported.
- ligation of RANK on DC cell surfaces is not only a survival stimulus, but also induces a partial and specific mature DC phenotype
- Ineffective modulation of the OPG/RANK/RANKL system in active polyarticular juvenile idiopathic arthritis may account for bone damage in this disease.
- might locally modulate [odontogenic] tumor-associated bone resorption
- Based on their role in atherogenesis, this enhanced expression of RANKL and RANK could contribute to the increased risk of cardiovascular disease in hyperhomocystinemia
- RANKL/RANK have roles in bone-associated tumors (review)