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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-related chemo (zeige IL8 Proteine)kines were identif (zeige CCL1 Proteine)ied 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
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.
Report a synthetic lethal interaction of cetuximab in combination with MEK1 (zeige MAP2K1 Proteine)/2 inhibition for the NRAS mutant subgroup of metastatic colorectal cancer.
NRAS was identified as a direct target of let-7e and promoted oncogenesis in glioma stem cells.
It may be that NRAS Q61R, found in around half of GCMNs, is a less potent promoter of FGF23 (zeige FGF23 Proteine) than the HRAS (zeige HRAS Proteine) mutations usually found in verrucous EN with CSHS, and requires a larger mutant clone to cause CSHS.
Study showed that NRAS-mutation(+) colorectal cancer (CRC (zeige CALR Proteine)) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC (zeige CALR Proteine) significantly correlated with less lymph vessel invasion, occurred preferentially in elder patients and at the distal colon, and showed relatively better prognosis, compared with KRAS-mutation(+) CRC (zeige CALR Proteine).
Oncogene (zeige RAB1A Proteine) NRAS G138R variant was identified as having a predicted damaging effect on protein function.
Results show that promoter mutations render telomerase reverse transcriptase (TERT (zeige TERT Proteine)) expression dependent on MAPK (zeige MAPK1 Proteine) signal pathway activation due to oncogenic BRAF (zeige BRAF Proteine) or NRAS mutations.
Mutational activation of Kit-, Ras/Raf (zeige RAF1 Proteine)/Erk (zeige EPHB2 Proteine)- and Akt (zeige AKT1 Proteine)- pathways indicate the biological importance of these pathways and their components as potential targets for therapy.
An age-related increase on the frequency of NRAS mutations was observed.
Melanomas from geographically different regions in New Zealand have markedly different mutation frequencies, in particular in the NRAS and EPHB6 (zeige EPHB6 Proteine) genes, when compared to The Cancer Genome Atlas database or other populations. These data have implications for the causation and treatment of malignant melanoma in New Zealand.
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