NRAS Antibodies

Structure of NRAS

The NRAS gene encodes a small GTP-binding protein with a molecular weight of approximately 21 kDa, and its size is highly conserved across different species. This protein belongs to the RAS family and is composed of 189 amino acids, featuring a highly specific sequence and structure. The tertiary structure of the NRAS protein shows a typical G-domain folding, consisting of six β -sheets and five α -helices, and its effector factor binding region is closely related to the GTP/GDP binding state. Amino acids at positions 12, 13 and 61 are common mutation hotspots. Variations at these key sites can lead to the loss of GTPase activity, keeping the protein in an activated state continuously and subsequently triggering excessive activation of downstream signaling pathways. The stability of this molecular conformation plays a decisive role in the occurrence and development of tumors.

Fig. 1 In silico structural analysis of NRAS Q61K and E132K with reference to NRAS WT.¹

Key structural properties of NRAS:

• Classical G-domain folding of the RAS family
• Highly conserved GTP/GDP binding region
• Amino acids at positions 12, 13 and 61 are high-frequency mutation hotspots

Functions of NRAS

The main function of the NRAS gene is to act as a molecular switch to regulate cell growth and proliferation signals. Its specific functions include:

NRAS shares highly similar effector protein binding regions with proteins of the same family (such as HRAS and KRAS), but the differences in their tissue expression specificity and mutation spectra lead to different carcinogenic pathological mechanisms. The NRAS mutant protein significantly weakened the GAP-induced hydrolysis reaction, resulting in the loss of GTPase activity and the continuous activation of the signal.

Applications of NRAS and NRAS Antibody in Literature

1. Giannou, Anastasios D., et al. "NRAS destines tumor cells to the lungs." EMBO molecular medicine 9.5 (2017): 672-686. https://doi.org/10.15252/emmm.201606978

Studies have found that NRAS mutations promote the interaction between tumor cells and pulmonary blood vessels and myeloid cells by regulating the expression of IL-8-related chemokines, and drive the targeting process of lung cancer metastasis. Inhibiting this chemokine signal can effectively block lung metastasis mediated by NRAS.

2. Ekvall, Sara, et al. "Mutation in NRAS in familial Noonan syndrome–case report and review of the literature." BMC medical genetics 16.1 (2015): 95.https://doi.org/10.1186/s12881-015-0239-1

Research has found that the c.179G>A mutation of the NRAS gene leads to Noonan syndrome, with clinical manifestations including freckles, cafe-au-lait spots and hearing loss. No significant increase in the risk of juvenile myelomonocytic leukemia has been observed, highlighting its correlation with pigmentation lesions.

3. Valentín-Bravo, Francisco Javier, et al. "Análise do valor prognóstico dos marcadores BRAF e NRAS no melanoma da conjuntiva e revisão da literatura." Arquivos Brasileiros de Oftalmologia 86.5 (2023): 1-6. https://doi.org/10.5935/0004-2749.20230071

Research has found that the mutation rates of NRAS and BRAF in conjunctival melanoma are both 25%, which are significantly associated with high tumor recurrence rates and systemic metastasis, and are important risk factors and potential therapeutic targets for poor prognosis.

4. Pang, Jia Meng, et al. "MicroRNA-708 emerges as a potential candidate to target undruggable NRAS." PLoS One 18.4 (2023): e0284744.https://doi.org/10.1371/journal.pone.0284744

Research has found that miRNA-708 specifically inhibits the expression of mutant proteins in the 3'utr region of the NRAS gene by targeting it, thereby blocking downstream signaling pathways, providing a new precise treatment strategy for NRAS-driven cancers.

5. Lian, Shen-Yi, et al. "KRAS, NRAS, BRAF signatures, and MMR status in colorectal cancer patients in North China." Medicine 102.9 (2023): e33115.https://doi.org/10.1097/MD.0000000000033115

This study analyzed 369 patients with colorectal cancer, and the NRAS mutation rate was 1.6%. KRAS mutations and mismatch repair deficits (dMMR) are associated with clinical features such as tumor location and differentiation, and dMMR is a positive prognostic indicator. However, KRAS mutations predict a poorer overall survival period for patients in stage IV.

Creative Biolabs: NRAS Antibodies for Research

Creative Biolabs specializes in the production of high-quality NRAS antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom NRAS Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our NRAS antibodies, custom preparations, or technical support, contact us at email.