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抗Rat (Rattus) GTPase NRas 抗体:
抗Mouse (Murine) GTPase NRas 抗体:
抗Human GTPase NRas 抗体:
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 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 Monoclonal GTPase NRas Primary Antibody for WB - ABIN1882272
Hall, Brown: Human N-ras: cDNA cloning and gene structure. in Nucleic acids research 1985
A sequential and coordinated activation of ERK (显示 EPHB2 抗体), JNK (显示 MAPK8 抗体) and STAT3 (显示 STAT3 抗体) with RACK1 (显示 GNB2L1 抗体) is shown to accelerate aggressive melanoma development in vivo.
MEK1 (显示 MAP2K1 抗体) does not act as a general tumor suppressor in leukemogenesis. Rather, its effects strongly depend on the genetic context (RAS versus MYC (显示 MYC 抗体)-driven leukemia) and on the cell type involved.
our data indicate that endogenous NrasQ61R/+ induces an increase of Nras-GTP (显示 AK3 抗体) and cytokine-evoked signaling, which is intermediate between NrasG12D/+ and NrasG12D/G12D
Interleukin-8-related chemo (显示 IL8 抗体)kines were identif (显示 CCL1 抗体)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 抗体) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (显示 HRAS 抗体) 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 抗体), after exposure to urethane.
Genetic inactivation of Ezh2 (显示 EZH2 抗体) or Eed (显示 EED 抗体) 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 抗体) 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
Mutation analysis Iindicate NRAS as the most commonly mutated gene in myeloma patients followed by KRAS ( and BRAF (显示 BRAF 抗体).
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 (显示 BRAF 抗体) mutated patient treated with a BRAF (显示 BRAF 抗体) inhibitor were identified post-resistant samples. Sequence analysis showed that NRAS mutations co-occur with BRAF (显示 BRAF 抗体) mutations in single cells, and are not mutually exclusive.
studies suggest that ZDHHC9 (显示 ZDHHC9 抗体) 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 (显示 MAP2K1 抗体)/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 (显示 FGF23 抗体) than the HRAS (显示 HRAS 抗体) 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 抗体)) had distinct epigenetic and clinicopathological features and significantly correlated with low-methylation epigenotypes. NRAS-mutation(+) CRC (显示 CALR 抗体) 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 抗体).
Oncogene (显示 RAB1A 抗体) 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 抗体)) expression dependent on MAPK (显示 MAPK1 抗体) signal pathway activation due to oncogenic BRAF (显示 BRAF 抗体) or NRAS mutations.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (显示 TP53 抗体) 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