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Validated All-in-One™ qPCR Primer for NRAS(NM_002524.4) Search again
Product ID:
HQP054878
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALPS4, CMNS, KRAS, N-ras, NCMS, NRAS1, NS6
Gene Description:
NRAS proto-oncogene, GTPase
Target Gene Accession:
NM_002524.4(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 is an N-ras oncogene encoding a membrane protein that shuttles between the Golgi apparatus and the plasma membrane. This shuttling is regulated through palmitoylation and depalmitoylation by the ZDHHC9-GOLGA7 complex. The encoded protein, which has intrinsic GTPase activity, is activated to a GTP-bound form by a GTPase activating protein and inactivated to a GDP-bound form by a guanine nucleotide-exchange factor. Defects in this gene are a cause of juvenile myelomonocytic leukemia (JMML). [provided by RefSeq].
Gene References into function
- Mutations were detected by using allele-specific amplification method.
- BMECs co-expressing SV40T, hTERT and N-ras exhibited an overtly transformed phenotype; forming very large colonies with an altered morphology and generating rapidly growing tumours in vivo.
- Regulation of Fas-mediated apoptosis by N-ras in melanoma.
- Protein kinase C mediates mutant N-Ras-induced developmental abnormalities erythropoiesis, giving rise to phenotypic and functional abnormalities commonly observed in preleukemia.
- role of interleukin-6 in activation of expression
- HDL induced a potent signal through a Ras/MAPK pathway mediated by a pertussis toxin-sensitive G-protein coupled receptor to the angiogenic phenotype in HCECs.
- high frequency of NRAS codon 61 mutations detected in primary hereditary melanomas may be the result of a hypermutability phenotype associated with a hereditary predisposition for melanoma development in patients with germline CDKN2A mutations
- NRAS and BRAF mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression
- Acquisition of N-ras mutation is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia
- Mutations in N-ras gene is associated with malignant melanomas
- Data show that Golgi-associated N-Ras is the critical Ras isoform and intracellular pool for low-grade T cell receptor signaling in Jurkat T cells.
- Low frequency of NRAS and KRAS2 gene mutations in childhood myelodysplastic syndromes.
- NRAS mutations are frequent in acute myeloblastic leukemia with normal karyotype.
- oncogenic NRAS is important for avoidance of apoptosis in melanomas that harbor the codon 61 NRAS mutation
- Although BRAF and NRAS mutations are likely to be important for the initiation and maintenance of some melanomas, other factors might be more significant for proliferation and prognosis in subgroups of aggressive melanoma
- Overactivation of N-Ras61K induces cytoplasmic mislocalization of p27 and disrupts TGF-beta-mediated Smad nuclear translocation by activation of the Mek/Erk pathway.
- Ras mutations do not play a significant role in the pathogenesis of multiple myeloma in the Spanish population
- NRAS and BRAF activating mutations can coexist in the same melanoma, but are mutually exclusive at the single-cell level
- In 239 Thai adult AML cases, 35 RAS mutations were found in 32 cases (13%) predominantly classified as M1/M2 (53%) followed by M4/M5 (38%). Ten cases were positive for NRAS codon 12, 11 for NRAS codon 61, 13 for NRAS codon 13, and one for KRAS codon 13.
- ras may be involved in early stages of larynx carcinogenesis and may be activated by other mechanisms different from mutations, such as epigenetic events
- NRAS mutation is associated with melanoma and melanocytic nevi.
- The chemical properties and stucture of the membrane bound C-terminus of N-ras is reported.
- Ras gene mutations, mostly involving the N-Ras gene, were detected in 20% of the multiple myeloma patients; Ras gene mutations are not likely to represent a master lesion in MM
- NRAS mutations were associated with a significantly higher Clark level of invasion in melanoma tumours
- Our data suggest that the activity of specific RAS isoforms is context-dependent and provide a possible explanation for the prevalence of NRAS mutations in melanoma.
- patients having juvenile myelomonocytic leukemia with NRAS or KRAS2 glycine to serine substitution received no chemotherapy, but hematologic improvement was observed during a 2- to 4-year follow up
- data indicate that both early-life UV exposure and nevus propensity contribute to occurrence of BRAF+ melanoma, whereas nevus propensity and later-life sun exposure influence the occurrence of NRAS+ melanoma
- observations on the effects of NRAS activation indicate that RAS-inactivating drugs, such as farnesyltransferase inhibitors should be examined in human autoimmune and lymphocyte homeostasis disorders
- Nras gene mutation might be one of the mechanisms of oncogenesis of lung adenocarcinoma.
- No mutations in NRAS was found in pilocytic astrocytomas.
- Ras mutations were found in 33% of the papillary thyroid carcinomas
- CD155, at least in part, enhances the proliferation of ras-mutated cells
- expression of RET, nuclearRAS, and ERK proteins is greatly enhanced in papillary thyroid carcinoma cells and Hashimoto's thyroiditis oxyphil cells.
- Frequently mutated in high hyperdiploid childhood acute lymphoblastic leukemia.
- Data indicate that a critical component of Ras signaling is the activation of PLD.
- 54% of childhood CBF-AML had RTKs and/or Ras mutations
- 16k PRL inhibits cell migration by blocking the Ras-Tiam1-Rac1-Pak1 signaling pathway in endothelial cells
- mutation of N-RAS or B-RAF, signature genetic lesions present in most MMs, potently induced the expression of cell-surface CD200, a repressor of DC function.
- NRAS mutation is not associated with cutaneous melanoma
- N-ras mutation is associated with familial non-medullary thyroid carcinoma
- restricting CDC25A can limit tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell division or viability [review]
- the Ras-Net (Elk-3) pathway involves microtubules and is inhibited by pyrazoles
- Mitogen-activated protein kinase (MAPK) activity is subject to regulation even in BRAF/NRAS mutant melanoma cells and that high MAPK pathway signaling may be important only in distinct subsets of tumor cells.
- NRAS mutation is associated with disease stabilization in melanoma
- AML patients carrying mutRAS benefit from higher cytarabine doses more than wtRAS patients. This seems to be the first example of an activating oncogene mutation favorably modifying response to higher drug doses in AML.
- Silencing of N-Ras gene expression using shRNA decreases transformation efficiency and tumor growth in transformed cells induced by anti-BPDE.
- co-overexpression of KIT/CDK4 is a potential mechanism of oncogenic transformation in some BRAF/NRAS wild-type melanomas
- analysis of a signaling mechanism for the regulation of the Ras/ERK pathway based on the eNOS-dependent differential activation of N-Ras and K-Ras at specific cell compartments
- N-RAS(Q61K) and B-RAF(V600E) contribute to melanoma's resistance to apoptosis in part by downregulating Bim expression
- Mutation in NRAS is associated with childhood acute lymphoblastic leukemia
- Stimulation of human mast cells by activated T cells leads to N-Ras activation through Ras guanine nucleotide releasing protein 1.
- suppression of oncogenic NRAS by siRNA can induce growth arrest and inhibit invasion of human melanoma cells by modulating the levels of these gene products