mProX™ Human NRAS Stable Cell Line

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;Hep3B;PLC

Target Classification

Kinase Cell Lines

Target Research Area

Autoimmune Research

Related Diseases

Ras-Associated Autoimmune Leukoproliferative Disorder; Noonan Syndrome 6

Gene ID

Human:4893

UniProt ID

Human:P01111

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

NRAS (Neuroblastoma RAS viral oncogene homolog) is a gene that plays a role in various cancers, including acute myeloid leukemia (AML), myeloproliferative neoplasms (MPNs), colorectal adenocarcinoma, and conjunctival melanoma. In AML, the DUSP1 signaling pathway, which is regulated by NRAS, has been found to be associated with cytarabine (Ara-C) resistance. Knockdown of DUSP1 sensitizes AML cells to Ara-C treatment. In MPNs, NRAS mutations are correlated with the progression of the disease. In colorectal adenocarcinoma, NRAS mutation status is one of the molecular markers used to guide therapy. In conjunctival melanoma, biomarkers such as NRAS mutations have been identified and may be targeted for future therapies. Overall, NRAS has implications in the sensitivity to treatment and progression of various cancers.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Morgan Garcia (Verified Customer)

What is the impact of NRAS mutations on the efficacy of immunotherapy in melanoma? Mar 31 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

NRAS mutations can influence the response rates and prognosis of advanced melanoma treated with anti-PD-1 monotherapy. Mar 31 2023

chat Morgan Brown (Verified Customer)

Are there effective therapies for NRAS mutant melanoma? Mar 29 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

Yes, there are therapeutic options focusing on combined inhibition of MAPK signaling and CDK4/6-driven cell cycle progression for NRAS mutant melanoma. Mar 29 2020

Published Data

Fig.1 Knockdown of NRAS in HCC cell lines.

Hep3B and PLC cell lines of hepatocellular carcinoma (HCC) were subjected to transfection for a duration of 48 hours using two distinct si-RNA-pools: a control si-RNA-pool (Control) and another si-RNA-pool specifically targeting NRAS mRNA (si-NRAS). Subsequently, the levels of NRAS mRNA and protein were assessed, accompanied by the inclusion of representative Western blot illustrations to highlight statistically significant differences (*: P<.05) compared to the control group.

Ref: Dietrich, Peter, et al. "Neuroblastoma RAS viral oncogene homolog (NRAS) is a novel prognostic marker and contributes to sorafenib resistance in hepatocellular carcinoma." Neoplasia 21.3 (2019): 257-268.

Pubmed: 30685691

DOI: 10.1016/j.neo.2018.11.011

Research Highlights

Chen, Dong; K, Olga. "Genomic alterations in blast phase of BCR::ABL1-negative myeloproliferative neoplasms." International journal of laboratory hematology, 2023.
The blast phase of BCR::ABL1-negative myeloproliferative neoplasm (MPN-BP) is the final stage of the disease, characterized by complex genomic alterations. These alterations are caused by changes in DNA and RNA sequences, resulting in either the gain or loss of function of various encoded proteins. These proteins, including adaptor proteins, enzymes, components of spliceosomes, cell cycle checkpoints regulators, transcription factors, and proteins in cell signaling pathways, can be affected at different levels such as transcription, translation, and post-translational modification. Mutated genes such as ASXL1, EZH2, IDH1, IDH2, TET2, SRSF2, U2AF1, TP53, NRAS, KRAS, PTPN11, SH2B3/LNK, and RUNX1 play significant roles at various stages of genetic material expression, modification, and protein function in MPNs. These mutations have been linked to the progression of MPN-BP. In this review, the common mutational profiles, functions, and associations of these genes with the development of MPN-BP are summarized.
Chen, Dong; K, Olga. "Genomic alterations in blast phase of BCR::ABL1-negative myeloproliferative neoplasms." International journal of laboratory hematology, 2023.
Pubmed: 37867386 DOI: 10.1111/ijlh.14184

Karimpour, Mina. et al. "Pathway-driven analysis of synthetic lethal interactions in cancer using perturbation screens." Life science alliance, 2024.
The concept of synthetic lethality has shown potential for developing effective treatments for cancer in cases where targeting specific driver genes is not feasible. The current study utilized a newly developed computational framework to analyze various screenings and identify potential synthetic lethal (SL) interactions in pan-cancer and 12 specific cancer types. By incorporating biological function and pathway information of key driver genes, this approach was able to minimize the impact of underlying genetic alterations in different cancer cell lines. The results revealed numerous putative SL interactions which can guide future research efforts.
Karimpour, Mina. et al. "Pathway-driven analysis of synthetic lethal interactions in cancer using perturbation screens." Life science alliance, 2024.
Pubmed: 37863651 DOI: 10.26508/lsa.202302268