Recombinant Human GTPase NRas (NRAS)

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Code CSB-EP016070HU
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Greater than 85% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Alternative Names
ALPS4; AV095280; GTPase NRas; HRAS1; N ras; N ras protein part 4; Neuroblastoma RAS viral (v ras) oncogene homolog; NRAS; NRAS1; NS6; OTTHUMP00000013879; OTTMUSP00000023521; RASN_HUMAN; Transforming protein N Ras; Transforming protein N-Ras; v ras neuroblastoma RAS viral oncogene homolog
Homo sapiens (Human)
Expression Region
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
56.1 kDa
Protein Length
Full Length of Mature Protein
Tag Info
N-terminal 10xHis-GST-tagged and C-terminal Myc-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

NRAS is a protein that acts as a messenger inside cells, initiating the MAPK signaling pathway [1]. It belongs to a group of proteins called RAS, which help cells respond to growth signals [2]. In healthy cells, NRAS proteins switch between different forms, one active and the other inactive [3]. But when mutations happen, especially at a spot called codon 61, in about 30% of melanomas, NRAS gets stuck in the "on" position, accelerating the MAPK pathway and AKT pathway, which drives melanoma growth [4][5]. About one-fifth of melanomas have these overactive NRAS genes, which keep cells multiplying uncontrollably [6].

These mutant NRAS proteins kick off a domino effect, activating other pathways like MAPK, PI3K/AKT/mTOR, and Ral, leading to uncontrolled cell growth and tumor formation [4][6]. Blocking certain proteins involved in NRAS activity can slow down cell growth in blood cells with NRAS mutations [7]. Recent treatments for NRAS mutant melanomas target these downstream pathways, like MAPK and PI3K, as well as proteins that regulate cell division [8]. The main players affected by NRAS in melanoma include RAFs (ARAF, BRAF, and CRAF), phosphatidylinositol 3-kinase (PI3K), and RAS-like protein (RAL) GEFs [9].

[1] S. Balaratnam, Z. Torrey, D. Calabrese, M. Banco, K. Yazdani, X. Lianget al., "Investigating the nras 5’ utr as a target for small molecules",, 2022.
[2] F. Janku, A. Kaseb, A. Tsimberidou, R. Wolff, & R. Kurzrock, "Identification of novel therapeutic targets in the pi3k/akt/mtor pathway in hepatocellular carcinoma using targeted next generation sequencing", Oncotarget, vol. 5, no. 10, p. 3012-3022, 2014.
[3] X. Chen, G. Tang, J. Dai, L. Dai, T. Wu, W. Liet al., "Discovery of clinically used octenidine as nras repressor that effectively inhibits nras-mutant melanoma", Journal of Medicinal Chemistry, vol. 66, no. 7, p. 5171-5184, 2023.
[4] T. Kim, J. Kim, & M. Lee, "Inhibition of mutated braf in melanoma", New England Journal of Medicine, vol. 363, no. 23, p. 2261-2262, 2010.
[5] T. Whitwam, V. Mw, R. Me, H. Pt, D. Bilgili, R. Jhet al., "Differential oncogenic potential of activated ras isoforms in melanocytes", Oncogene, vol. 26, no. 31, p. 4563-4570, 2007.
[6] I. Vujic, M. Sanlorenzo, C. Posch, R. Esteve-Puig, A. Yen, A. Kwonget al., "Metformin and trametinib have synergistic effects on cell viability and tumor growth innrasmutant cancer", Oncotarget, vol. 6, no. 2, p. 969-978, 2014.
[7] I. Vujic, M. Sanlorenzo, R. Esteve-Puig, M. Vujic, A. Kwong, A. Tsumuraet al., "Acyl protein thioesterase 1 and 2 (apt-1, apt-2) inhibitors palmostatin b, ml348 and ml349 have different effects on nras mutant melanoma cells", Oncotarget, vol. 7, no. 6, p. 7297-7306, 2016.
[8] C. Posch, B. Cholewa, I. Vujic, M. Sanlorenzo, J. Ma, S. Kimet al., "Combined inhibition of mek and plk1 has synergistic antitumor activity in nras mutant melanoma", Journal of Investigative Dermatology, vol. 135, no. 10, p. 2475-2483, 2015.
[9] H. Vu and A. Aplin, "Targeting mutant nras signaling pathways in melanoma", Pharmacological Research, vol. 107, p. 111-116, 2016.

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Target Background

Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
Gene References into Functions
  1. Tet2/Nras double-mutant leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples PMID: 29275866
  2. Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS PMID: 29495918
  3. NRAS mutations harbor commonly in neurocutaneous melanosis. PMID: 30145692
  4. Ets-1 is induced by BRAF or MEK kinase inhibition, resulting in increased NRAS expression, which could be blocked by inactivation of Usp9x. PMID: 28198367
  5. we used hot-spot mutation sequencing to examine whether KRAS/NRAS mutations, a characteristic feature of mesonephric carcinoma,1 are also present in mesonephric hyperplasia. None of the mesonephric hyperplasia cases harboured a KRAS or NRAS mutation. PMID: 28703285
  6. BRAF mutations more frequently affected individuals younger than 61 with phototype II. In contrast, NRAS mutations were more frequent in phototype III cases. Mutations of both genes were more frequent in cases with satellitosis in the first melanoma, and in cases with ulceration in the subsequent lesions. PMID: 29180316
  7. Identification of KRAS/NRAS/BRAF mutation status is crucial to predict the therapeutic effect and determine individual therapeutic strategies for patients with colorectal cancer. PMID: 29335867
  8. common conjunctival melanocytic nevi have mutually exclusive mutations in BRAF and NRAS. The two conjunctival blue nevi harbored GNAQ mutations. This suggests the driver mutations of conjunctival nevi are similar to those of nevi of the skin. At the molecular level, conjunctival nevi appear more like cutaneous nevi than choroidal nevi PMID: 29332123
  9. the mutational status of BRAF, NRAS, and TERT promoter genes in 97 melanomas, was investigated. PMID: 29061376
  10. Deciphering KRAS and NRAS mutated clone dynamics in MLL-AF4 paediatric leukaemia by ultra deep sequencing analysis. PMID: 27698462
  11. N-Ras preferentially populated raft domains when bound to mant-GDP. It lost its preference for rafts when associated with a GTP mimic, mant-GppNHp. The isolated lipidated C-terminal peptide of N-Ras was outside of the liquid-ordered rafts, most likely in the bulk-disordered lipid. Substitution of the N-Ras N-terminal G domain with a homologous G domain of H-Ras disrupted the nucleotide-dependent lipid domain switch. PMID: 29280621
  12. We report herein for the first time that 30% of cutaneous NRAS mutant melanomas have a high M%NRAS. Chromosome instability, (chromosome 1 polysomy, intratumor copy number variation of chromosome1/NRAS) rather than the acquired copy neutral LOH seems to be responsible for most of the cases with high M%NRAS. PMID: 28668077
  13. NRAS status (exons 2-4) was analyzed by Pyrosequencing in a case series of 50 squamous cell anal carcinoma patients. PMID: 27886225
  14. NRAS-mutant tumors tended to behave more aggressively particularly in early stages of the disease in studied high-risk melanoma population. PMID: 28797232
  15. Data show that mutations in NRAS are associated with poor survival. PMID: 28446505
  16. Authors analyzed 421 samples from CLM patients for their all-RAS mutation status to compare the overall survival rate (OS), recurrence-free survival rate (RFS), and the pattern of recurrence between the patients with and without RAS mutations. PMID: 29194647
  17. The lack of KRAS, NRAS, BRAF, and PIK3CA mutation in our study may suggest that a subset of eyelid sebaceous carcinomas is unlike that of eyelid sebaceous carcinomas of western countries. PMID: 28551389
  18. in vitro assays confirmed that decreased miR-425 strongly induced inflammatory cytokines (interleukin [IL]-2 and interferon [IFN]-gamma) via N-Ras upregulation in the TCR signalling pathway in primary biliary cholangitis PMID: 28192189
  19. analysis of NRAS mutations in pulmonary Langerhans cell histiocytosis PMID: 27076591
  20. analysis of K-RAS and N-RAS mutations in testicular germ cell tumors PMID: 28426398
  21. KRAS mutations were rarely found together and those in codons 12 and 13 conferred poor prognosis. For BRAF, more c.1781A>G (p.D594G) colorectal cancers (CRC)carried RAS mutations [14% (3/21)] compared with c.1799T>A (p.V600E) CRCs.For NRAS, 5% (3/60) of codon 61 mutant colorectal cancers had KRAS mutations compared with 44% (10/23) of codons 12 and 13 mutant colorectal cancers PMID: 27815357
  22. Mutation analysis Iindicate NRAS as the most commonly mutated gene in myeloma patients followed by KRAS ( and BRAF. PMID: 27634910
  23. A rapid monophyletic evolution of melanoma subpopulations in response to targeted therapy that was not observed in non-targeted therapy was observed. NRAS mutations in BRAF mutated patient treated with a BRAF inhibitor were identified post-resistant samples. Sequence analysis showed that NRAS mutations co-occur with BRAF mutations in single cells, and are not mutually exclusive. PMID: 27791198
  24. studies suggest that ZDHHC9 may serve as a safe and effective target for developing therapies against NRAS-driven cancers PMID: 26493479
  25. MEK1 does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC-driven leukemia) and on the cell type involved. PMID: 27741509
  26. Report a synthetic lethal interaction of cetuximab in combination with MEK1/2 inhibition for the NRAS mutant subgroup of metastatic colorectal cancer. PMID: 27636997
  27. NRAS was identified as a direct target of let-7e and promoted oncogenesis in glioma stem cells. PMID: 27556696
  28. It may be that NRAS Q61R, found in around half of GCMNs,[9] is a less potent promoter of FGF23 than the HRAS mutations usually found in verrucous EN with CSHS, and requires a larger mutant clone to cause CSHS. PMID: 27900779
  29. Study showed that NRAS-mutation(+) colorectal cancer (CRC) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC significantly correlated with less lymph vessel invasion, occurred preferentially in elder patients and at the distal colon, and showed relatively better prognosis, compared with KRAS-mutation(+) CRC. PMID: 28378457
  30. Oncogene NRAS G138R variant was identified as having a predicted damaging effect on protein function. PMID: 27121310
  31. NRASQ61R Mutation-specific Immunohistochemistry is Highly Specific for Either NRASQ61R or KRASQ61R Mutation in Colorectal Carcinoma. PMID: 26862952
  32. Results show that promoter mutations render telomerase reverse transcriptase (TERT) expression dependent on MAPK signal pathway activation due to oncogenic BRAF or NRAS mutations. PMID: 27449293
  33. Mutational activation of Kit-, Ras/Raf/Erk- and Akt- pathways indicate the biological importance of these pathways and their components as potential targets for therapy. PMID: 27391150
  34. An age-related increase on the frequency of NRAS mutations was observed. PMID: 27433783
  35. Melanomas from geographically different regions in New Zealand have markedly different mutation frequencies, in particular in the NRAS and EPHB6 genes, when compared to The Cancer Genome Atlas database or other populations. These data have implications for the causation and treatment of malignant melanoma in New Zealand. PMID: 27191502
  36. Data indicate acquired KRAS, NRAS or HRAS mutations in more than one third of patients after cetuximab exposure. PMID: 27119512
  37. Mutational status of NRAS, KRAS, and PTPN11 genes is associated with genetic/cytogenetic features in children with B-precursor acute lymphoblastic leukemia. PMID: 28853218
  38. The results demonstrated the lack of activity of anti-EGFRs in RAS(KRAS and NRAS) and BRAF wild-type, right-sided tumors, thus suggesting a potential role for primary tumor location in driving treatment choices PMID: 27382031
  39. Data indicate that BRAF, NRAS and C-KIT melanomas constitute distinct clinico-pathological entities. PMID: 29187493
  40. NRAS promotes interleukin-8-related chemokine secretion by tumor cells. PMID: 28341702
  41. MC1R genotype is associated with patient phenotypes with BRAF and NRAS mutations in melanoma PMID: 28842324
  42. Our data suggest that KRAS, NRAS, and BRAF mutations predict response to cetuximab treatment in metastatic colorectal cancer patients. PMID: 26989027
  43. Although recurrent NRAS mutations are present, the low mutation rate suggests that NRAS itself plays a minor role in the development of low-grade ovarian serous carcinoma. PMID: 28873354
  44. Results show that NRAS mRNA is a direct target of microRNA miR-340. PMID: 26799668
  45. complex signaling mechanisms that involve PREX2, PI3K/AKT/PTEN and downstream epigenetic machinery to deregulate expression of key cell cycle regulators PMID: 27111337
  46. he rapid tumor onset observed in this replication attempt, compared to the original study, makes the detection of accelerated tumor growth in PREX2 expressing NRAS(G12D) melanocytes extremely difficult. PMID: 28100394
  47. Mutations in KRAS, NRAS, and BRAF together occur in more than half of all colorectal cancer cases and are often associated with negative responses to the EGFR inhibitors cetuximab and panitumumab.guideline is clear that we should not be giving EGFR inhibitors to patients with RAS mutations and that patients with BRAF V600E mutations have a much worse prognosis PMID: 28249840
  48. KIT knockdown increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant melanoma cell line. PMID: 28947418
  49. NRAS mutation is associated with response to therapy in rectal cancer. PMID: 28859058
  50. Age at diagnosis of follicular thyroid cancer (FTC) and frequency of extrathyroidal extension have changed over four decades; prevalence of RAS mutations has decreased; HRAS/NRAS (codon 61) and TERT (promoter) mutations may be associated with poor clinical outcomes in FTC, especially when two mutations coexist; this retrospective study was conducted in Seoul. PMID: 28864536

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Involvement in disease
Leukemia, juvenile myelomonocytic (JMML); Noonan syndrome 6 (NS6); RAS-associated autoimmune leukoproliferative disorder (RALD); Melanocytic nevus syndrome, congenital (CMNS); Melanosis, neurocutaneous (NCMS); Keratinocytic non-epidermolytic nevus (KNEN); Thyroid cancer, non-medullary, 2 (NMTC2)
Subcellular Location
Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus membrane; Lipid-anchor.
Protein Families
Small GTPase superfamily, Ras family
Database Links

HGNC: 7989

OMIM: 137550

KEGG: hsa:4893

STRING: 9606.ENSP00000358548

UniGene: Hs.486502

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