Mutations in RAS and various components of the Ras signaling pathways are among the most common causative genetic alterations in human cancers, accounting up to 25% of lung cancers and over 90% of pancreatic cancers. Ras is a small GTPase that functions as a ‘molecular switch’ in a number of signaling pathways that regulate vital eukaryotic cellular functions. Despite our comprehensive understanding of the molecular mechanisms governing the activity of Ras, the clinical outcome of various pharmacologic anti-cancer strategies designed to directly inactivate Ras have been less than satisfactory. In this review, the more recently uncovered mode of regulation of Ras involving non-receptor tyrosine kinase and phosphatase, which have long been suspected of contributing to the oncogenic potential of Ras, will be discussed in the context of both function and structure.
Page:
S1084952116301689
Related
Batch download
Cited By
noting
Similar Literature
Submit Feedback
Please wait while the file you selected is being converted