Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Rat (Rattus) GTPase NRas Anticorps:
anti-Mouse (Murine) GTPase NRas Anticorps:
anti-Human GTPase NRas Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal GTPase NRas Primary Antibody pour ELISA, WB - ABIN544419
Banerji, Affolter, Judson, Marais, Workman: BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors. dans Molecular cancer therapeutics 2008
Show all 2 Pubmed References
Dog (Canine) Polyclonal GTPase NRas Primary Antibody pour 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. dans Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2007
Human Monoclonal GTPase NRas Primary Antibody pour WB - ABIN1882272
Hall, Brown: Human N-ras: cDNA cloning and gene structure. dans Nucleic acids research 1985
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.
These observations provide genetic evidence for an essential role of Ras proteins in the control of keratinocyte and epidermal proliferation.
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.
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.
Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS
NRAS mutations harbor commonly in neurocutaneous melanosis.
Ets-1 is induced by BRAF or MEK kinase inhibition, resulting in increased NRAS expression, which could be blocked by inactivation of Usp9x.
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.
BRAF mutations more frequently affected individuals younger than 61 with phototype II. In contrast, NRAS mutations were more frequent in phototype III cases. Mutations of both genes were more frequent in cases with satellitosis in the first melanoma, and in cases with ulceration in the subsequent lesions.
Identification of KRAS/NRAS/BRAF mutation status is crucial to predict the therapeutic effect and determine individual therapeutic strategies for patients with colorectal cancer.
common conjunctival melanocytic nevi have mutually exclusive mutations in BRAF and NRAS. The two conjunctival blue nevi harbored GNAQ mutations. This suggests the driver mutations of conjunctival nevi are similar to those of nevi of the skin. At the molecular level, conjunctival nevi appear more like cutaneous nevi than choroidal nevi
the mutational status of BRAF, NRAS, and TERT promoter genes in 97 melanomas, was investigated.
Deciphering KRAS and NRAS mutated clone dynamics in MLL-AF4 paediatric leukaemia by ultra deep sequencing analysis.
N-Ras preferentially populated raft domains when bound to mant-GDP. It lost its preference for rafts when associated with a GTP mimic, mant-GppNHp. The isolated lipidated C-terminal peptide of N-Ras was outside of the liquid-ordered rafts, most likely in the bulk-disordered lipid. Substitution of the N-Ras N-terminal G domain with a homologous G domain of H-Ras disrupted the nucleotide-dependent lipid domain switch.
We report herein for the first time that 30% of cutaneous NRAS mutant melanomas have a high M%NRAS. Chromosome instability, (chromosome 1 polysomy, intratumor copy number variation of chromosome1/NRAS) rather than the acquired copy neutral LOH seems to be responsible for most of the cases with high M%NRAS.
NRAS status (exons 2-4) was analyzed by Pyrosequencing in a case series of 50 squamous cell anal carcinoma patients.
NRAS-mutant tumors tended to behave more aggressively particularly in early stages of the disease in studied high-risk melanoma population.
Data show that mutations in NRAS are associated with poor survival.
In the title.
Authors analyzed 421 samples from CLM patients for their all-RAS mutation status to compare the overall survival rate (OS), recurrence-free survival rate (RFS), and the pattern of recurrence between the patients with and without RAS mutations.
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