NRAS KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1 and 2 bp deletion in exon1 and 5 bp deletion in exon1.
ALPS4, AV095280, GTPase NRas, H-Ras-1, N ras, N ras protein part 4, NRAS1, NS6, Neuroblastoma RAS viral (v ras) oncogene homolog, OTTHUMP00000013879, OTTMUSP00000023521, RASN_HUMAN, Transforming protein N-Ras, v ras neuroblastoma RAS viral oncogene homolog
NRAS KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1 and 2 bp deletion in exon1 and 5 bp deletion in exon1.
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Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our limited use license and patent pages.
The NRAS protein also known as neuroblastoma RAS viral oncogene homolog has a molecular weight of approximately 24 kDa. It functions mechanically as a GTPase cycling between an inactive GDP-bound state and an active GTP-bound state. The NRAS gene which encodes this protein shows expression in various tissues including the thymus leukocytes and other cells of the hematopoietic lineage. Activation of RAS involves the conversion to the GTP-bound form which enables NRAS to transmit signals within cells.
NRAS plays an important role in cell proliferation differentiation and survival. It does not function alone but is part of the larger RAS protein family including HRAS and KRAS with whom it shares similar roles and sequence homology. NRAS interacts with various growth factor receptors and mediates signals to downstream effectors that influence cellular processes. Mutations in the NRAS gene can affect these biological processes leading to altered cell behavior.
NRAS has significant roles in the MAPK/ERK pathway and the PI3K/AKT pathway. These pathways regulate fundamental cellular functions including growth and survival. NRAS interacts closely with other proteins such as RAF kinases and PI3K to propagate signals from activated receptors at the cell membrane to the nucleus. Altered NRAS activity can impact these pathways affecting cellular responses to external stimuli.
NRAS mutations are linked to certain cancers including melanoma and acute myeloid leukemia (AML). Mutant forms of NRAS result in constitutively activated RAS contributing to uncontrolled cell growth and survival. In melanoma NRAS mutations frequently co-occur with alterations in other proteins such as BRAF another member of the RAS/RAF/MEK/ERK pathway. Understanding NRAS's involvement in these conditions is critical for developing targeted therapeutic strategies.
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Allele-3: 5 bp deletion in exon1
Allele-1: 2 bp deletion in exon1
Allele-2: 1 bp insertion in exon1
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