What Are the Consequences of Ras Mutation
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- Category: Politics: Political Science
- Date Submitted: 01/06/2011 01:00 PM
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Consequences Of Ras Mutation
Mutations in the three closely related ras genes, H-ras, K-ras, and N-ras, are among the most common mutations found in human cancer, reaching 50% in some types of tumors, such as colorectal carcinoma. Mutations of the K-Ras gene occur in over 90% of pancreatic carcinomas. The ras pathway is important in the transmission of growth-promoting signals from the cell surface receptors, eventually toward the nucleus where these signals affect the production and regulation of other key proteins
Most mutations in genes are expected to cause their inactivation, however, in the Ras genes the opposite happens - they become more active in signaling. This is because of the engineering design of the protein. The ras signal is turned off by a molecular switch, which depends on an enzyme activity. In picturesque terms, the nucleotide GTP (guanidine triphosphate) engages the switch to keep it in the "on" state. A portion of the Ras protein has an enzyme activity (a GTPase) which cleaves the GTP. This turns the switch "off" after the brief "on" period. In reality, the mutations of Ras do indeed inactivate a function, as most mutations are expected to do. The GTPase is inactivated by the mutations. But this now means that GTP continues to engage the switch, and the Ras signaling function is unable to be turned "off
Ras mutations involve only certain amino acids, those which interfere with the GTPase function. In pancreatic cancer, mutations are essentially seen only at the twelfth position, (codon or amino acid 12), with rare exceptions seen at codon 13. Most mutations in pancreatic cancer change a glycine at codon 12 to a valine or aspartate. The mutation to serine is quite unusual in pancreatic cancer, a peculiar finding since it is a common mutation in other tumor types which have K-ras mutations.
Mutations in K-ras occur early in the development of colon carcinoma. This dominantly acting mutation in ras results in its constitutive activation and...
Mutations in the three closely related ras genes, H-ras, K-ras, and N-ras, are among the most common mutations found in human cancer, reaching 50% in some types of tumors, such as colorectal carcinoma. Mutations of the K-Ras gene occur in over 90% of pancreatic carcinomas. The ras pathway is important in the transmission of growth-promoting signals from the cell surface receptors, eventually toward the nucleus where these signals affect the production and regulation of other key proteins
Most mutations in genes are expected to cause their inactivation, however, in the Ras genes the opposite happens - they become more active in signaling. This is because of the engineering design of the protein. The ras signal is turned off by a molecular switch, which depends on an enzyme activity. In picturesque terms, the nucleotide GTP (guanidine triphosphate) engages the switch to keep it in the "on" state. A portion of the Ras protein has an enzyme activity (a GTPase) which cleaves the GTP. This turns the switch "off" after the brief "on" period. In reality, the mutations of Ras do indeed inactivate a function, as most mutations are expected to do. The GTPase is inactivated by the mutations. But this now means that GTP continues to engage the switch, and the Ras signaling function is unable to be turned "off
Ras mutations involve only certain amino acids, those which interfere with the GTPase function. In pancreatic cancer, mutations are essentially seen only at the twelfth position, (codon or amino acid 12), with rare exceptions seen at codon 13. Most mutations in pancreatic cancer change a glycine at codon 12 to a valine or aspartate. The mutation to serine is quite unusual in pancreatic cancer, a peculiar finding since it is a common mutation in other tumor types which have K-ras mutations.
Mutations in K-ras occur early in the development of colon carcinoma. This dominantly acting mutation in ras results in its constitutive activation and...