Herbie is a typical American college freshman who loves to eat. His second most favorite food is hotdogs. He cuts them into his Kraft macaroni and cheese at a 1:1 ratio, going through a score of hotdogs each week. He doesn't know his brand is preserved with sodium nitrite, but his stomach is slowly finding out as it's acid converts the sodium nitrite to nitrous acid, a weak mutagen. In the lining of Herbie's stomach three little cells each experience a mutation in their DNA and it happens to be in the very same gene--a kinase gene called src. (Src is an example of what Dr. Howard Temin called a "proto-oncogene.) But the three little cells each experienced a different kind of mutation in that gene:
Cell #1's src DNA was altered so that it's product is present in normal amounts, but no longer functions.
Cell #2's src DNA was altered so that it produces almost no gene product at all.
Cell #3's src DNA was altered so that it's gene product has normal function but is overproduced.© BrainMass Inc. brainmass.com October 16, 2018, 7:38 pm ad1c9bdddf
Cell #3's src DNA was altered so that it's gene product has normal ...
Src kinase overproduction resulting in cancer.
This figure is from Bose et al. 2006 [see attached[ (A) What can be concluded with respect to the regulation of PLCy1, STAT1, DOK1, o-Cat, AXL and FYB by the Her2 receptor. (B) In general, what is the mechanism that regulates how proteins interact with the Her2 receptor? (C) What is different about how the signal for PLCy1 phosphorylation was generated compared to that for DOK1 phosphorylation?
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