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A sequential and coordinated activation of ERK (zeige EPHB2 Proteine), JNK (zeige MAPK8 Proteine) and STAT3 (zeige STAT3 Proteine) with RACK1 (zeige GNB2L1 Proteine) is shown to accelerate aggressive melanoma development in vivo.
MEK1 (zeige MAP2K1 Proteine) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (zeige MYC Proteine)-driven leukemia) and on the cell type involved.
our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP (zeige AK3 Proteine) and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D
Interleukin-8 (zeige IL8 Proteine)-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 (zeige HRAS Proteine) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (zeige HRAS Proteine) allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras (zeige HRAS Proteine), after exposure to urethane.
Genetic inactivation of Ezh2 (zeige EZH2 Proteine) or Eed (zeige EED Proteine) 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 (zeige WNT2 Proteine) 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
BRAF (zeige BRAF Proteine) 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 (zeige BRAF Proteine) 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 (zeige BRAF Proteine), NRAS, and TERT (zeige TERT Proteine) 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 (zeige AK3 Proteine) 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 (zeige HRAS Proteine) 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.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (zeige TP53 Proteine) 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