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Validated All-in-One™ qPCR Primer for NOG(NM_005450.4) Search again
Powered by BiozBy 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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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 secreted polypeptide, encoded by this gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, this protein may have a principal role in creating morphogenic gradients. The protein appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation.
Gene References into function
- A novel NOG gene mutation giving rise to the (P35S) amino acid substitution has been identified in an Italian family with symphalangism.
- Autosomal dominant stapes ankylosis with broad thumbs and toes, hyperopia, and skeletal anomalies is caused by heterozygous nonsense and frameshift mutations in NOG, the gene encoding noggin
- crystal structure of the antagonist Noggin bound to BMP-7, which shows that Noggin inhibits BMP signalling by blocking the molecular interfaces of the binding epitopes for both type I and type II receptors
- Nog gene is connected to stapes ankylosis.
- Here, we show that the overexpression of human noggin, by acting to inhibit glial differentiation by subependymal progenitor cells, can potentiate adenoviral BDNF-mediated recruitment of new neurons to the adult rat neostriatum
- Mutations in the nog gene have been identified.
- These studies highlight the critical role played by Cys168 in noggin's biological activities.
- Overexpression of noggin in PC-3 cells inhibited the expansion of the lesion in vivo.
- Data show calcium-sensing receptor stimulation of T-84 epithelia and colonic myofibroblasts downregulated the BMP family antagonist Noggin.
- Lack of noggin expression by cancer cells may be a relevant mechanism contributing to the osteoblast response in bone metastases
- Antagonism of bone morphogenetic protein signaling by transgenic Noggin plays a critical role in ensuring proper levels of cell proliferation and epithelial-to-mesenchymal transformation during cardiac morphogenesis.
- Expression analysis of additional genes, AKT1, NOG and its antagonist BMP4, which interact downstream to FGFR1, demonstrated expression differences between primary rhabdomyosarcoma tumors and normal skeletal muscles
- NOG is involved in myeloproliferative disease associated with myelofibrosis
- Various mutations may occur in myositis ossificans nuclear families.
- Heterozygous gene mutations in NOGGIN are associated with tall stature in children but not necessarily in adults.
- Advanced melanoma cells may escape from BMP7-induced inhibition through concomitant aberrant expression of Noggin.
- the potential use of bone-morphogenetic protein-6, noggin and sclerostin expression together as a prognostic predictor for metastatic progression of prostate cancer.