Recombinant Human Gtpase Nras (NRAS) Protein (His-GST&Myc)

Name: Recombinant Human Gtpase Nras (NRAS) Protein (His-GST&Myc)
Brand: Beta LifeScience
SKU: BLC-04756P
Availability: InStock

Greater than 85% as determined by SDS-PAGE.

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Product Overview

Description	Recombinant Human Gtpase Nras (NRAS) Protein (His-GST&Myc) is produced by our E.coli expression system. This is a full length protein.
Purity	Greater than 85% as determined by SDS-PAGE.
Uniprotkb	P01111
Target Symbol	NRAS
Synonyms	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
Species	Homo sapiens (Human)
Expression System	E.coli
Tag	N-10His-GST&C-Myc
Target Protein Sequence	MTEYKLVVVGAGGVGKSALTIQLIQNHFVDEYDPTIEDSYRKQVVIDGETCLLDILDTAGQEEYSAMRDQYMRTGEGFLCVFAINNSKSFADINLYREQIKRVKDSDDVPMVLVGNKCDLPTRTVDTKQAHELAKSYGIPFIETSAKTRQGVEDAFYTLVREIRQYRMKKLNSSDDGTQGCMGLPC
Expression Range	1-186aa
Protein Length	Full Length of Mature Protein
Mol. Weight	56.1 kDa
Research Area	Cancer
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function	Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
Subcellular Location	Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus membrane; Lipid-anchor.
Protein Families	Small GTPase superfamily, Ras family
Database References	HGNC: 7989 OMIM: 137550 KEGG: hsa:4893 STRING: 9606.ENSP00000358548 UniGene: PMID: 29275866 Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS PMID: 29495918 NRAS mutations harbor commonly in neurocutaneous melanosis. PMID: 30145692 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 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 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 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 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 the mutational status of BRAF, NRAS, and TERT promoter genes in 97 melanomas, was investigated. PMID: 29061376 Deciphering KRAS and NRAS mutated clone dynamics in MLL-AF4 paediatric leukaemia by ultra deep sequencing analysis. PMID: 27698462 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 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 NRAS status (exons 2-4) was analyzed by Pyrosequencing in a case series of 50 squamous cell anal carcinoma patients. PMID: 27886225 NRAS-mutant tumors tended to behave more aggressively particularly in early stages of the disease in studied high-risk melanoma population. PMID: 28797232 Data show that mutations in NRAS are associated with poor survival. PMID: 28446505 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 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 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 analysis of NRAS mutations in pulmonary Langerhans cell histiocytosis PMID: 27076591 analysis of K-RAS and N-RAS mutations in testicular germ cell tumors PMID: 28426398 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 Mutation analysis Iindicate NRAS as the most commonly mutated gene in myeloma patients followed by KRAS ( and BRAF. PMID: 27634910 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 studies suggest that ZDHHC9 may serve as a safe and effective target for developing therapies against NRAS-driven cancers PMID: 26493479 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 Report a synthetic lethal interaction of cetuximab in combination with MEK1/2 inhibition for the NRAS mutant subgroup of metastatic colorectal cancer. PMID: 27636997 NRAS was identified as a direct target of let-7e and promoted oncogenesis in glioma stem cells. PMID: 27556696 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 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 Oncogene NRAS G138R variant was identified as having a predicted damaging effect on protein function. PMID: 27121310 NRASQ61R Mutation-specific Immunohistochemistry is Highly Specific for Either NRASQ61R or KRASQ61R Mutation in Colorectal Carcinoma. PMID: 26862952 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 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 An age-related increase on the frequency of NRAS mutations was observed. PMID: 27433783 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 Data indicate acquired KRAS, NRAS or HRAS mutations in more than one third of patients after cetuximab exposure. PMID: 27119512 Mutational status of NRAS, KRAS, and PTPN11 genes is associated with genetic/cytogenetic features in children with B-precursor acute lymphoblastic leukemia. PMID: 28853218 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 Data indicate that BRAF, NRAS and C-KIT melanomas constitute distinct clinico-pathological entities. PMID: 29187493 NRAS promotes interleukin-8-related chemokine secretion by tumor cells. PMID: 28341702 MC1R genotype is associated with patient phenotypes with BRAF and NRAS mutations in melanoma PMID: 28842324 Our data suggest that KRAS, NRAS, and BRAF mutations predict response to cetuximab treatment in metastatic colorectal cancer patients. PMID: 26989027 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 Results show that NRAS mRNA is a direct target of microRNA miR-340. PMID: 26799668 complex signaling mechanisms that involve PREX2, PI3K/AKT/PTEN and downstream epigenetic machinery to deregulate expression of key cell cycle regulators PMID: 27111337 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 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 KIT knockdown increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant melanoma cell line. PMID: 28947418 NRAS mutation is associated with response to therapy in rectal cancer. PMID: 28859058 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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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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