Use your antibodies-online credentials, if available.
Select your species
Interleukin-8-related chemo (显示 IL8 ELISA试剂盒)kines were identif (显示 CCL1 ELISA试剂盒)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 (显示 HRAS ELISA试剂盒) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (显示 HRAS ELISA试剂盒) allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras (显示 HRAS ELISA试剂盒), after exposure to urethane.
Genetic inactivation of Ezh2 (显示 EZH2 ELISA试剂盒) or Eed (显示 EED ELISA试剂盒) 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 (显示 WNT2 ELISA试剂盒) 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 (显示 RUNX1 ELISA试剂盒) cell lines in vitro and for the maintenance of mouse Nras-mutant AML (显示 RUNX1 ELISA试剂盒) in vivo
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 (显示 FGF23 ELISA试剂盒) than the HRAS (显示 HRAS ELISA试剂盒) 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 (显示 CALR ELISA试剂盒)) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC (显示 CALR ELISA试剂盒) 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 (显示 CALR ELISA试剂盒).
Oncogene (显示 RAB1A ELISA试剂盒) NRAS G138R variant was identified as having a predicted damaging effect on protein function.
Results show that promoter mutations render telomerase reverse transcriptase (TERT (显示 TERT ELISA试剂盒)) expression dependent on MAPK (显示 MAPK1 ELISA试剂盒) signal pathway activation due to oncogenic BRAF (显示 BRAF ELISA试剂盒) or NRAS mutations.
Mutational activation of Kit-, Ras/Raf (显示 RAF1 ELISA试剂盒)/Erk (显示 EPHB2 ELISA试剂盒)- and Akt (显示 AKT1 ELISA试剂盒)- 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 (显示 EPHB6 ELISA试剂盒) 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.
Data indicate acquired KRAS, NRAS or HRAS (显示 HRAS ELISA试剂盒) mutations in more than one third of patients after cetuximab exposure.
Mutational status of NRAS, KRAS, and PTPN11 (显示 PTPN11 ELISA试剂盒) genes is associated with genetic/cytogenetic features in children with B-precursor acute lymphoblastic leukemia.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (显示 TP53 ELISA试剂盒) 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