Description
Key facts
Purity:>95% HPLC,
Endotoxin level:<0.1 EU/mg,
Expression system:Escherichia coli,
Tags:His tag N-Terminus,
Applications:SDS-PAGE, Mass SpecSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Biologically active:No,
Accession:P01111,
Animal free:Yes,
Carrier free:No,
Species:Human,
Storage buffer:pH: 7Constituents: 20% Glycerol (glycerin, glycerine), 1.4586% Sodium chloride, 0.2691% Disodium hydrogenorthophosphate, 0.1629% Sodium Phosphate Monobasic, 0.0148% (R*,R*)-1,4-Dimercaptobutan-2,3-diol
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--80°C, Appropriate long-term storage conditions--80°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
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.
Biological function summary
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.
Pathways
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.
