Browse our anti-GTPase NRas (NRAS) Antibodies

Mouse (Murine) GTPase NRas (NRAS) interaction partners

1. Oncogenic N-Ras and Tet2 haploinsufficiency collaborate to dysregulate hematopoietic stem and progenitor cells.

2. Tet2/Nras double-mutant leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples

3. Results indicate specific and compensatory functions for proto-oncogene B-Raf (BRAF) and proto-oncogene c-RAF (CRAF) and highlight an addiction to RAF signalling in NRAS-driven melanoma.

4. gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a full developmental time course, are reported.

5. A sequential and coordinated activation of ERK, JNK and STAT3 with RACK1 is shown to accelerate aggressive melanoma development in vivo.

6. 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.

7. our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D

8. Interleukin-8-related chemokines were identified as the tumor cell-secreted culprits for NRAS-dependent pulmonary metastatic propensity, signaling to lung endothelial and myeloid cells to facilitate pulmonary invasion.

9. complex signaling mechanisms that involve PREX2, PI3K/AKT/PTEN and downstream epigenetic machinery to deregulate expression of key cell cycle regulators

10. loss of one allele of Hras increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras, after exposure to urethane.

11. Genetic inactivation of Ezh2 or Eed cooperates with NRASQ61K in leukemogenesis.

12. Data indicate that S-phase kinase-associated protein 2 (SKP2) cooperates with N-Ras and AKT proto-oncogenes to promote hepatocarcinogenesis in vivo.

13. Activated NRAS and aberrant Wnt signaling conspire to drive congenital melanocytic nevus syndrome.

14. a crucial role of RXRa in suppression of UVB-induced melanomas in the context of driver mutations such as activated CDK4(R24C/R24C) or oncogenic NRAS(Q61K) and altered expression of p53 and PTEN

15. This work explains the curious predominance in human melanoma of mutations of codon 61 of NRAS over other oncogenic NRAS mutations. we show that physiologic expression of NRASQ61R, but not NRASG12D, drives melanoma formation.

16. These data reveal the L. major-enhanced CD40-induced N-Ras activation as a novel immune evasion strategy and the potential for Ras isoform-targeted antileishmanial immunotherapy and immunoprophylaxis.

17. NRAS expression is required for the proliferative advantage of human AML cell lines in vitro and for the maintenance of mouse Nras-mutant AML in vivo

18. There was a nearly complete correspondence between the signaling pathways that were regulated by N-ras in immune cell types.

19. Cbfbeta-SMMHC and Nras(G12D) promote the survival of preleukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define Nras(LSL-G12D); Cbfb(56M) mice as a valuable genetic model for the study of AML therapies.

20. regulation of Nf1 exon 23a inclusion serves as a mechanism for providing appropriate levels of Ras signaling.

Human GTPase NRas (NRAS) interaction partners

1. High NRAS isoform 5 expression is associated with malignant melanoma.

2. BRAF and NRAS mutations in Langerhans cell histiocytosis (LCH) suggest a possibility of the disease being driven by the activation of the MAPK/ERK pathway. These oncogenic mutations provide new opportunities in understanding LCH pathogenesis and may be a potential target of therapy

3. Two patients harbored KRAS with codon 12 mutations; one harbored the gly12val mutation with a variation of leu597val in the BRAF exon 15 codon, the other harbored mutation in the BRAF exon 15 codon. One patient harbored a codon 117 mutation with a BRAF V600E mutation. The last patient harbored a NRAS exon 2 mutation with the GGT/GAT, V600G mutation in the BRAF exon 15 codon

4. The study shows a high concordance of KRAS, NRAS, BRAF and PIK3CA gene mutations in plasma against mutation status in tumor tissue.

5. FLT3-ITD was the most common mutated gene (16.2%, 42/259), followed by CEBPA (15.1%, 39/259), NRAS (14.7%, 38/259), and NPM1 (13.5%, 35/259). The results showed certain rules in the mutation profiling and concurrence of acute myeloid leukemia (AML) patients, which was related to the function classification of genes.

6. No mutation was found in the NRAS gene in our patients

7. NRAS found to be overexpressed in hepatocellular carcinoma (HCC) cell lines, preclinical HCC models, and human HCC tissues. NRAS overexpression correlated with poor survival and proliferation in vivo. NRAS expression was elevated in sorafenib-resistant compared to nonresistant HCC cells, and NRAS knockdown enhanced sorafenib efficacy in resistant cells.

8. NRAS mutation c.181C>A (p.Gln61Lys) is associated with congenital nevus syndrome.

9. The Q61R mutation of the NRAS gene is one of the most frequent driver mutations of thyroid cancer. The expression of NRAS(Q61R) in thyroid epithelial cells has a profound influence on groups of genes involved in the formation of intercellular contacts, as well as in processes of epithelial-mesenchymal transition and cell invasion.

10. These findings highlight a novel mechanism for resistance to ER-stress through oncogenic activation of MEK/ERK signalling by RAC1 and NRAS.

11. The primary aim of this study was to explore if patients with BRAF or NRAS mutant tumours compared to patients with wild-type tumours have an increased risk of developing disease recurrence following a negative sentinel lymph node biopsy (SLNB)

12. Ectopic introduction of SPRY4 recapitulated the growth arrest phenotype of dual BRAF(V600E)/NRAS(Q61) expression while SPRY4 depletion led to a partial rescue from oncogenic antagonism.

13. bFGF-mediated pluripotency maintenance in human induced pluripotent stem cells is associated with NRAS-MAPK signaling

14. introducing a rapid and sensitive microarray-based assay for the multiplex detection of minority mutations of oncogenes (KRAS, NRAS and BRAF) with relevant diagnostics implications in tissue biopsies and plasma samples in metastatic colorectal cancer patients

15. Gene mutations in BRAF, MSI-high status, and N-ras differ according to gender among patients with colorectal cancer

16. The results suggest it is likely that all acquired naevi will be mutated for NRAS, thus supporting the role of the MAPK pathway in the development of benign melanocytic proliferations. These data confirm that additional genomic events besides somatic mutations in NRAS are required for melanoma development.

17. NRAS gene could predict the poor prognosis for the CRC patients.

18. MicroRNA-22 targeted NRAS proto-oncogene.

19. A robust dependency of NRAS-mutant melanoma on TERT.

20. Low NRAS expression is associated with Pancreatic Adenocarcinoma.

Zebrafish GTPase NRas (NRAS) interaction partners

1. Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 was found to collaborate with NRAS expression in the genesis of melanoma.