NRAS Antibody (YA6200)
(Synonyms: HRAS1, NRAS, GTPase NRas, Transforming protein N-Ras)Based on 1 Customer Validation
NRAS Antibody (YA6200) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to NRAS.
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Host:
Rabbit
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Isotype:
IgG/Kappa
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Application:
WB, IHC-P, ICC/IF, IP, ELISA
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|---|
| Dilution Ratio | 1:200-1:1000 | 1:1000-1:5000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 |
Product Details
NRAS Antibody (YA6200) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to NRAS.
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Host Rabbit
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 22 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 22 kDa
Protein A
Non-conjugated
Unmodified
IgG/Kappa
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
N-Ras is a small GTPase that controls cell proliferation, differentiation, and survival through GDP/GTP-regulated signaling[1]. Mechanistically, Ras proteins cycle between ON and OFF states and signal through effector pathways including RAF-MEK-ERK and PI3K[2][3]. In disease models, NRAS has strong relevance in melanoma and acute myelogenous leukemia, and NRAS-mutant melanoma depends on MAPK and PI3K/mTOR signaling[4][5]. Compared with related isoforms, N-Ras, K-Ras, and H-Ras share high G-domain conservation, but biochemical studies show distinct catalytic and signaling properties, so H-Ras data should not be treated as fully representative of N-Ras[1][6]. Isoform distinction also matters experimentally because KRAS is usually more abundant than NRAS in cell-line panels, whereas NRAS often exceeds HRAS in those models[7]. For applications, MEK inhibition with binimetinib improved progression-free survival versus dacarbazine in advanced NRAS-mutant melanoma, while combined MEK and PI3K/mTOR targeting showed antitumor activity in NRAS-mutant melanoma models[8][5]. Recent NRAS-directed monobody work further supports direct inhibition and degradation strategies for NRAS-focused research tools[9].
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Subcellular Localization
Cell membrane; Lipid-anchor; Cytoplasmic side; Golgi apparatus membrane; Lipid-anchor
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Subunit
Interacts (active GTP-bound form preferentially) with RGS14 (By similarity). Interacts (active GTP-bound form) with RASSF7 (PubMed:21278800). Interacts (active GTP-bound form) with both SHOC2 and PP1c (all isoforms) to form a tertiary complex; SHOC2 and PP1c preferably bind M-Ras/MRAS, but they also bind K-Ras/KRAS, N-Ras/NRAS and H-Ras/HRAS (PubMed:36175670, PubMed:35768504, PubMed:35831509, PubMed:35830882)
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SwissProt ID
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Synonyms
HRAS1, NRAS, GTPase NRas, Transforming protein N-Ras
Documentation
[1]. Johnson CW, et al. The small GTPases K-Ras, N-Ras, and H-Ras have distinct biochemical properties determined by allosteric effects. J Biol Chem. 2017 Aug 4;292(31):12981-12993. [Content Brief]
[2]. Simanshu DK, et al. RAS Proteins and Their Regulators in Human Disease. Cell. 2017 Jun 29;170(1):17-33. [Content Brief]
[3]. Castellano E, et al. RAS Interaction with PI3K: More Than Just Another Effector Pathway. Genes Cancer. 2011 Mar;2(3):261-74. [Content Brief]
[4]. Johnson DB, et al. Molecular pathways: targeting NRAS in melanoma and acute myelogenous leukemia. Clin Cancer Res. 2014 Aug 15;20(16):4186-92. [Content Brief]
[5]. Posch C, et al. Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo. Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):4015-20. [Content Brief]
[6]. Castellano E, et al. Functional specificity of ras isoforms: so similar but so different. Genes Cancer. 2011 Mar;2(3):216-31. [Content Brief]
[7]. Hood FE, et al. Ras protein abundance correlates with Ras isoform mutation patterns in cancer. Oncogene. 2023 Apr;42(15):1224-1232. [Content Brief]
[8]. Dummer R, et al. Binimetinib versus dacarbazine in patients with advanced NRAS-mutant melanoma (NEMO): a multicentre, open-label, randomised, phase 3 trial. Lancet Oncol. 2017 Apr;18(4):435-445. [Content Brief]
[9]. Whaby M, et al. Inhibition and degradation of NRAS with a pan-NRAS monobody. Oncogene. 2024 Nov;43(48):3489-3497. [Content Brief]
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