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anti-Rat (Rattus) GTPase NRas Antibodies:
anti-Mouse (Murine) GTPase NRas Antibodies:
anti-Human GTPase NRas Antibodies:
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Human Monoclonal GTPase NRas Primary Antibody for IHC (p), WB - ABIN5584750
Oishi, Kondo, Vuong, Nakazawa, Mochizuki, Kasai, Inoue, Tahara, Hirokawa, Miyauchi, Katoh: Immunohistochemical detection of NRAS(Q61R) protein in follicular-patterned thyroid tumors. in Human pathology 2016
Human Polyclonal GTPase NRas Primary Antibody for IHC (p), IHC - ABIN409077
Thomas, Edmiston, Alexander, Millikan, Groben, Hao, Tolbert, Berwick, Busam, Begg, Mattingly, Ollila, Tse, Hummer, Lee-Taylor, Conway: Number of nevi and early-life ambient UV exposure are associated with BRAF-mutant melanoma. in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2007
Human Monoclonal GTPase NRas Primary Antibody for WB - ABIN1882272
Hall, Brown: Human N-ras: cDNA cloning and gene structure. in Nucleic acids research 1985
Interleukin-8-related chemo (show IL8 Antibodies)kines were identif (show CCL1 Antibodies)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 (show DEPDC2 Antibodies), PI3K/AKT (show AKT1 Antibodies)/PTEN (show PTEN Antibodies) and downstream epigenetic machinery to deregulate expression of key cell cycle regulators
loss of one allele of Hras (show HRAS Antibodies) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (show HRAS Antibodies) 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 Antibodies), after exposure to urethane.
Genetic inactivation of Ezh2 (show EZH2 Antibodies) or Eed (show EED Antibodies) 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 Antibodies) signaling conspire to drive congenital melanocytic nevus syndrome.
a crucial role of RXRa (show RXRA Antibodies) in suppression of UVB-induced melanomas in the context of driver mutations such as activated CDK4 (show CDK4 Antibodies)(R24C/R24C) or oncogenic NRAS(Q61K) and altered expression of p53 (show TP53 Antibodies) and PTEN (show PTEN Antibodies)
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 Antibodies) cell lines in vitro and for the maintenance of mouse Nras-mutant AML (show RUNX1 Antibodies) 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 (show FGF23 Antibodies) than the HRAS (show HRAS Antibodies) 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 Antibodies)) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC (show CALR Antibodies) 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 Antibodies).
Oncogene (show RAB1A Antibodies) NRAS G138R variant was identified as having a predicted damaging effect on protein function.
Results show that promoter mutations render telomerase reverse transcriptase (TERT (show TERT Antibodies)) expression dependent on MAPK (show MAPK1 Antibodies) signal pathway activation due to oncogenic BRAF (show BRAF Antibodies) or NRAS mutations.
Mutational activation of Kit-, Ras/Raf (show RAF1 Antibodies)/Erk (show EPHB2 Antibodies)- and Akt (show AKT1 Antibodies)- 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 (show EPHB6 Antibodies) 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 (show HRAS Antibodies) mutations in more than one third of patients after cetuximab exposure.
Mutational status of NRAS, KRAS, and PTPN11 (show PTPN11 Antibodies) 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 (show TP53 Antibodies) 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