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Using one example of a cellular oncogene, illustrate molecular mechanisms of activation and the consequences for protein function; for this specific example, also provide information about the occurrence in cancer and any current treatments - Essay Example

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Majority of normal cells go through apoptosis, a process that is curtailed by activated oncogenes, causing them to survive and proliferate (Hanahan & Weinberg 2011, p…
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Using one example of a cellular oncogene, illustrate molecular mechanisms of activation and the consequences for protein function; for this specific example, also provide information about the occurrence in cancer and any current treatments
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"Using one example of a cellular oncogene, illustrate molecular mechanisms of activation and the consequences for protein function; for this specific example, also provide information about the occurrence in cancer and any current treatments"

Download file to see previous pages The oncogene is also involved in the regulation of diverse behaviors of the cell as part of the larger Ras protein super-family. Their signaling activity results in the growth and division of cells, which means that over-activity on the oncogene’s part, will ultimately cause cancer (Hanahan & Weinberg 2011, p. 654). In fact, the Ras oncogene is the most common in cancer with over 20% of all human cancers possessing permanent Ras mutations and 90% in some cancers like pancreatic cancer. Therefore, inhibitors of the Ras oncogene have been studied in the search for cancer treatment.
Ras is a protein that binds guanosine nucleotides and is referred to as G-protein. As with other G-proteins, Ras functions as a binary signaling switch with binding of GTP switching it on, while binding of GDP acts to switch it off. The additional phosphate functional group ensures that the switch regions are configured as a loaded spring at Gly-60 and Thr-35 (Weinberg 2013, p. 115). Therefore, the cycling between inactive GDP and active GTP molecules controls the deactivation and activation of the Ras oncogene. Exchange between these molecules is, in turn, facilitated by GEF and GAP molecules, of which GEF promotes the release of GDP and attachment of GTP to the Ras oncogene. Examples of GEF’s include cdc25 and Son of Sevenless (Bock & Marsh 2010, p. 65).
The GEF protein catalyzes the release of GDP by inserting near the binding sites for Mg+ and the P-loop, thus inhibiting their interaction with P-. Within the P-loop, a lysine group is pulled away from GDP by negative residues, increasing the distance between switch I and guanine, and breaking the contact between GDP and Ras (Bock & Marsh 2010, p. 65). Since there is an abundance of activated GTP molecules in the cell, it predominantly binds to the Ras molecule’s nucleotide binding site. In this configuration, the oncogene has heightened ...Download file to see next pagesRead More
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