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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
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 (show RUNX1 Proteins) cell lines in vitro and for the maintenance of mouse Nras-mutant AML (show RUNX1 Proteins) in vivo
There was a nearly complete correspondence between the signaling pathways that were regulated by N-ras in immune cell types.
Cbfbeta (show CBFB Proteins)-SMMHC (show MYH11 Proteins) and Nras(G12D) promote the survival of preleukemic myeloid progenitors primed for leukemia by activation of the MEK (show MDK Proteins)/ERK (show EPHB2 Proteins)/Bim (show BCL2L11 Proteins) axis, and define Nras(LSL-G12D); Cbfb (show CBFB Proteins)(56M) mice as a valuable genetic model for the study of AML (show RUNX1 Proteins) therapies.
NRAS mutation is associated with response to therapy in rectal cancer.
Age at diagnosis of follicular thyroid cancer (FTC (show FUT2 Proteins)) and frequency of extrathyroidal extension have changed over four decades; prevalence of RAS mutations has decreased; HRAS/NRAS (codon 61) and TERT (show TERT Proteins) (promoter) mutations may be associated with poor clinical outcomes in FTC (show FUT2 Proteins), especially when two mutations coexist; this retrospective study was conducted in Seoul.
No significant impact on prognosis was observed for mutated KRAS, NRAS, and PIK3CA genes or combined RAS mutations
BRAF (show BRAF Proteins) and NRAS mutations were associated with CNS and liver metastasis and NRAS mutation with lung metastasis.
Germline variants in NRAS causing RASopathy are characterized.
Authors found significant co-occurrence of mutations in NRAS and EIF1AX (show EIF1AX Proteins) Missense EIF1AX (show EIF1AX Proteins) mutations were clustered at the N-terminus of the protein in a region associated with its role in ensuring translational initiation fidelity.
NRAS mutations were present in 1.2% of primary papillary thyroid carcinomas, 1.3% of lymph node metastasis, and 14.3% of distant metastasis.
Data suggest that isoform-specific sequences in the allosteric lobes of HRAS (show HRAS Proteins), KRAS, and NRAS have an impact on biocatalysis (kinetics of GTP (show AK3 Proteins) hydrolysis) and interaction with c-Raf (show RAF1 Proteins) kinase, which must be due to allosteric effects on dynamics and conformational states, given the identical active sites of these isoenzymes.
NRAS(Q61R) immunohistochemistry is a highly sensitive and specific tool that is useful for differentiating follicular-patterned thyroid tumors.
NRAS variants were identified in 2 cases with a lethal presentation of Noonan syndrome.
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