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anti-Rat (Rattus) GTPase NRas Antibodies:
anti-Mouse (Murine) GTPase NRas Antibodies:
anti-Human GTPase NRas Antibodies:
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Human Polyclonal GTPase NRas Primary Antibody for ELISA, WB - ABIN544419
Banerji, Affolter, Judson, Marais, Workman: BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors. in Molecular cancer therapeutics 2008
Show all 2 Pubmed References
Human Monoclonal GTPase NRas Primary Antibody for IHC, WB - ABIN2727603
Potu, Peterson, Kandarpa, Pal, Sun, Durham, Harms, Hollenhorst, Eskiocak, Talpaz, Donato: Usp9x regulates Ets-1 ubiquitination and stability to control NRAS expression and tumorigenicity in melanoma. in Nature communications 2018
Human Monoclonal GTPase NRas Primary Antibody for WB - ABIN1882272
Hall, Brown: Human N-ras: cDNA cloning and gene structure. in Nucleic acids research 1985
Dog (Canine) Polyclonal GTPase NRas Primary Antibody for IHC (p), ELISA - ABIN548088
Thomas, Edmiston, Alexander, Millikan, Groben, Hao, Tolbert, Berwick, Busam, Begg, Mattingly, Ollila, Tse, Hummer, Lee-Taylor, Conway: Number of nevi and early-life ambient UV exposure are associated with BRAF-mutant melanoma. in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2007
Oncogenic N-Ras and Tet2 haploinsufficiency collaborate to dysregulate hematopoietic stem and progenitor cells.
Tet2/Nras double-mutant leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples
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.
gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a full developmental time course, are reported.
A sequential and coordinated activation of ERK, JNK and STAT3 with RACK1 is shown to accelerate aggressive melanoma development in vivo.
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.
our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D
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.
complex signaling mechanisms that involve PREX2, PI3K/AKT/PTEN and downstream epigenetic machinery to deregulate expression of key cell cycle regulators
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.
Genetic inactivation of Ezh2 or Eed cooperates with NRASQ61K in leukemogenesis.
Data indicate that S-phase kinase-associated protein 2 (SKP2) cooperates with N-Ras and AKT proto-oncogenes to promote hepatocarcinogenesis in vivo.
Activated NRAS and aberrant Wnt signaling conspire to drive congenital melanocytic nevus syndrome.
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
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.
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.
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
There was a nearly complete correspondence between the signaling pathways that were regulated by N-ras in immune cell types.
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.
regulation of Nf1 exon 23a inclusion serves as a mechanism for providing appropriate levels of Ras signaling.
No mutation was found in the NRAS gene in our patients
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.
NRAS mutation c.181C>A (p.Gln61Lys) is associated with congenital nevus syndrome.
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.
These findings highlight a novel mechanism for resistance to ER-stress through oncogenic activation of MEK/ERK signalling by RAC1 and NRAS.
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)
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.
bFGF-mediated pluripotency maintenance in human induced pluripotent stem cells is associated with NRAS-MAPK signaling
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
Gene mutations in BRAF, MSI-high status, and N-ras differ according to gender among patients with colorectal cancer
A postzygotic NRAS mutation in a patient with Schimmelpenning syndrome.
CSF cytology diagnosis of NRAS-mutated primary leptomeningeal melanomatosis with neurocutaneous melanosis.
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.
NRAS gene could predict the poor prognosis for the CRC patients.
MicroRNA-22 targeted NRAS proto-oncogene.
A robust dependency of NRAS-mutant melanoma on TERT.
Low NRAS expression is associated with Pancreatic Adenocarcinoma.
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.
NRAS point mutation could be considered as evidence, consistent with a Pulmonary Langerhans' cell Histiocytosis diagnosis.
Comparatively to BRAF mutation, results found that NRAS mutations are frequent in the follicular variant of papillary thyroid carcinoma.
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.
This is an N-ras oncogene encoding a membrane protein that shuttles between the Golgi apparatus and the plasma membrane. This shuttling is regulated through palmitoylation and depalmitoylation by the ZDHHC9-GOLGA7 complex. The encoded protein, which has intrinsic GTPase activity, is activated by a guanine nucleotide-exchange factor and inactivated by a GTPase activating protein. Mutations in this gene have been associated with somatic rectal cancer, follicular thyroid cancer, autoimmune lymphoproliferative syndrome, Noonan syndrome, and juvenile myelomonocytic leukemia.
, transforming protein N-Ras
, neuroblastoma RAS viral (v-ras) oncogene homolog
, N-ras oncogene
, p21 protein
, N-ras protein part 4
, v-ras neuroblastoma RAS viral oncogene homolog
, ras p21
, N-ras oncogene p21
, neuroblastoma RAS viral oncogene-like protein
, neuroblastoma ras oncogene
, v-Ha-ras Harvey rat sarcoma viral oncogene homolog