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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 IHC (p), IHC - ABIN409077
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
Human Monoclonal GTPase NRas Primary Antibody for WB - ABIN1882272
Hall, Brown: Human N-ras: cDNA cloning and gene structure. in Nucleic acids research 1985
A sequential and coordinated activation of ERK (show EPHB2 Antibodies), JNK (show MAPK8 Antibodies) and STAT3 (show STAT3 Antibodies) with RACK1 (show GNB2L1 Antibodies) is shown to accelerate aggressive melanoma development in vivo.
MEK1 (show MAP2K1 Antibodies) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (show MYC Antibodies)-driven leukemia) and on the cell type involved.
our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP (show AK3 Antibodies) and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D
Interleukin-8 (show IL8 Antibodies)-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 (show HRAS Antibodies) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (show HRAS Antibodies) allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras (show HRAS Antibodies), after exposure to urethane.
Genetic inactivation of Ezh2 (show EZH2 Antibodies) or Eed (show EED Antibodies) 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 (show WNT2 Antibodies) 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
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 (show BRAF Antibodies), NRAS, and TERT (show TERT Antibodies) 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 (show AK3 Antibodies) 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 (show HRAS Antibodies) 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.
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.
Findings indicate neurofibromin 1 (NF1 (show NF1 Antibodies)) as the most frequently occurring driver mutation in mucosal melanoma, and RAS alterations, consisting of NRAS and KRAS mutations, were the second most frequent mutation type.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (show TP53 Antibodies) 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