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Interleukin-8-related chemo (zeige IL8 ELISA Kits)kines were identif (zeige CCL1 ELISA Kits)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 (zeige HRAS ELISA Kits) increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras (zeige HRAS ELISA Kits) allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras (zeige HRAS ELISA Kits), after exposure to urethane.
Genetic inactivation of Ezh2 (zeige EZH2 ELISA Kits) or Eed (zeige EED ELISA Kits) 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 (zeige WNT2 ELISA Kits) 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 (zeige RUNX1 ELISA Kits) cell lines in vitro and for the maintenance of mouse Nras-mutant AML (zeige RUNX1 ELISA Kits) in vivo
Melanomas from geographically different regions in New Zealand have markedly different mutation frequencies, in particular in the NRAS and EPHB6 (zeige EPHB6 ELISA Kits) 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 (zeige HRAS ELISA Kits) mutations in more than one third of patients after cetuximab exposure.
Mutational status of NRAS, KRAS, and PTPN11 (zeige PTPN11 ELISA Kits) genes is associated with genetic/cytogenetic features in children with B-precursor acute lymphoblastic leukemia.
The results demonstrated the lack of activity of anti-EGFRs in RAS(KRAS and NRAS) and BRAF (zeige BRAF ELISA Kits) wild-type, right-sided tumors, thus suggesting a potential role for primary tumor location in driving treatment choices
IGF-II siRNA inactivates the FAK (zeige PTK2 ELISA Kits)/PI3K (zeige PIK3CA ELISA Kits)/Akt (zeige AKT1 ELISA Kits) signaling pathway, and further reduces cell proliferation, N-ras and C-myc (zeige MYC ELISA Kits) levels in SMMC-7721 cells.
Data indicate that BRAF (zeige BRAF ELISA Kits), NRAS and C-KIT (zeige KIT ELISA Kits) melanomas constitute distinct clinico-pathological entities.
NRAS promotes interleukin-8 (zeige IL8 ELISA Kits)-related chemokine (zeige CCL1 ELISA Kits) secretion by tumor cells.
MC1R (zeige MSHR ELISA Kits) genotype is associated with patient phenotypes with BRAF (zeige BRAF ELISA Kits) and NRAS mutations in melanoma
Our data suggest that KRAS, NRAS, and BRAF (zeige BRAF ELISA Kits) mutations predict response to cetuximab treatment in metastatic colorectal cancer patients.
Although recurrent NRAS mutations are present, the low mutation rate suggests that NRAS itself plays a minor role in the development of low-grade ovarian serous carcinoma.
Although oncogenic NRAS expression alone was found to be insufficient to promote tumor formation, loss of functional p53 (zeige TP53 ELISA Kits) 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