Description
Key facts
Species or organism:Human,
Form:LiquidSee storage information
Product details:
ab94323 is a 293T cell transfected lysate in which Human NPRL2 has been transiently over-expressed using a pCMV-NPRL2 plasmid. The lysate is provided in 1 x Sample Buffer.
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
NPRL2 also known as Nitrogen Permease Regulator-Like 2 plays a role in regulating the mTORC1 pathway. It is known to form part of the GATOR1 complex acting as a negative regulator of the mTORC1 signaling. NPRL2 has a molecular mass of approximately 41 kDa. This protein shows expression in various tissues with notable expression in the brain and lung.
Biological function summary
NPRL2 and its role in the GATOR1 complex importantly manages cellular response to nutrient availability and growth signals. The GATOR1 complex comprises NPRL2 NPRL3 and DEPDC5 which collectively suppress mTORC1 activity under nutrient-poor conditions. This suppression promotes autophagy and inhibits protein synthesis affecting how cells adapt to nutritional stress.
Pathways
NPRL2 is integral to the amino acid sensing branch of the mTORC1 signaling pathway. It plays a part in the nutrient sensing pathway alongside the proteins NPRL3 and DEPDC5. The mTORC1 pathway essential for controlling cell growth and metabolism depends on the regulated activity of NPRL2 and its partners to respond accurately to metabolic cues.
Altered NPRL2 function links to cancer and epilepsy. Mutations in the GATOR1 complex affecting proteins like DEPDC5 and NPRL3 in conjunction with NPRL2 have associations with tumor growth due to disrupted mTORC1 regulation. In epilepsy especially the focal cortical dysplasia type NPRL2 mutations lead to imbalanced mTORC1 activity contributing to the development of seizures.
