Recombinant Human KRAS (mutated G12C) Protein (His tag)

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The KRAS protein also known as Kirsten rat sarcoma viral oncogene homolog is a small GTPase weighing around 21 kDa. It plays an important role in cell signaling pathways and is widely expressed in various tissues. As a molecular switch KRAS cycles between an active GTP-bound state and an inactive GDP-bound state regulating cell proliferation differentiation and survival. KRAS mutations are often studied using various cell lines including the HCT116 line which is a human colorectal carcinoma cell line with a KRAS mutant background. Western blot analysis commonly helps in investigating KRAS protein expression and activity levels.

Biological function summary

KRAS influences many cellular processes. It is not part of a complex but acts alone within its pathways. It modulates signal transduction processes which are significant for the control of proliferation apoptosis and cell cycle progress. Mutations within this protein such as KRAS G12V and KRAS G12D lead to continuous activation and can cause uncontrolled cell growth which links them to various cancers. KRAS commonly interacts with proteins like RAF kinase and PI3K signaling components to execute its functions.

Pathways

KRAS is an important component in at least two important signaling pathways: the MAPK/ERK pathway and the PI3K/AKT pathway. These pathways play major roles in regulating gene expression that drives cell growth and division. In the MAPK/ERK pathway KRAS activates RAF which subsequently initiates a phosphorylation cascade that stimulates ERK. This protein also interacts with elements of the PI3K/AKT pathway influencing cellular survival and metabolism. These interactions position KRAS as a vital oncogene in cancer biology.

Associated diseases and disorders

KRAS mutations are important in the development and progression of colorectal and pancreatic cancers. The persistence of active KRAS leads to continuous signaling that drives tumor growth and resistance to apoptosis. KRAS-associated cancers often show poor prognosis partly due to limited therapeutic options. Its interaction with proteins like EGFR (Epidermal Growth Factor Receptor) in various cancers highlights complex treatment challenges as these proteins can provide alternative signaling routes further complicating disease management.