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. 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.

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

3. 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

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

5. A postzygotic NRAS mutation in a patient with Schimmelpenning syndrome.

6. CSF cytology diagnosis of NRAS-mutated primary leptomeningeal melanomatosis with neurocutaneous melanosis.

7. 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.

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

9. MicroRNA-22 targeted NRAS proto-oncogene.

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

11. Low NRAS expression is associated with Pancreatic Adenocarcinoma.

12. In Melanoma brain metastases (MBM), mutation status was not associated with distant brain failure overall survival. BRAF V600K and NRAS mutation status predict increased local brain failure following conventional treatments for MBM.

13. NRAS point mutation could be considered as evidence, consistent with a Pulmonary Langerhans' cell Histiocytosis diagnosis.

14. Comparatively to BRAF mutation, results found that NRAS mutations are frequent in the follicular variant of papillary thyroid carcinoma.

15. Studied NRAS and B-Raf proto-oncogene serine/threonine kinase (BRAF) mutations in Turkish cutaneous melanoma patients and their association with clinical stage of the melanomas.

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

17. Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS

18. NRAS mutations harbor commonly in neurocutaneous melanosis.

19. Ets-1 is induced by BRAF or MEK kinase inhibition, resulting in increased NRAS expression, which could be blocked by inactivation of Usp9x.

20. 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.

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.