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A sequential and coordinated activation of ERK (show EPHB2 Proteins), JNK (show MAPK8 Proteins) and STAT3 (show STAT3 Proteins) with RACK1 (show GNB2L1 Proteins) is shown to accelerate aggressive melanoma development in vivo.
MEK1 (show MAP2K1 Proteins) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (show MYC Proteins)-driven leukemia) and on the cell type involved.
our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP (show AK3 Proteins) and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D
Interleukin-8 (show IL8 Proteins)-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 Proteins) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (show HRAS Proteins) 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 Proteins), after exposure to urethane.
Genetic inactivation of Ezh2 (show EZH2 Proteins) or Eed (show EED Proteins) 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 Proteins) 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
KRAS mutations were rarely found together and those in codons 12 and 13 conferred poor prognosis. For BRAF, more c.1781A>G (p.D594G) colorectal cancers (CRC)carried RAS mutations [14% (3/21)] compared with c.1799T>A (p.V600E) CRCs.For NRAS, 5% (3/60) of codon 61 mutant colorectal cancers had KRAS mutations compared with 44% (10/23) of codons 12 and 13 mutant colorectal cancers
Mutation analysis Iindicate NRAS as the most commonly mutated gene in myeloma patients followed by KRAS ( and BRAF (show BRAF Proteins).
A rapid monophyletic evolution of melanoma subpopulations in response to targeted therapy that was not observed in non-targeted therapy was observed. NRAS mutations in BRAF (show BRAF Proteins) mutated patient treated with a BRAF (show BRAF Proteins) inhibitor were identified post-resistant samples. Sequence analysis showed that NRAS mutations co-occur with BRAF (show BRAF Proteins) mutations in single cells, and are not mutually exclusive.
studies suggest that ZDHHC9 (show ZDHHC9 Proteins) may serve as a safe and effective target for developing therapies against NRAS-driven cancers
Report a synthetic lethal interaction of cetuximab in combination with MEK1 (show MAP2K1 Proteins)/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 (show FGF23 Proteins) than the HRAS (show HRAS Proteins) 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 (show CALR Proteins)) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC (show CALR Proteins) 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 (show CALR Proteins).
Oncogene (show RAB1A Proteins) NRAS G138R variant was identified as having a predicted damaging effect on protein function.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (show TP53 Proteins) 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