There could be many reasons. One is Dcr2 is directly involved in DNA damage repair mechanism, so as the damage is induced, the need for Dcr2 increases. Another could be since dicer is an endoribonuclease, it has a role in making miRNAs that are needed for DNA damage response pathway.
For your future directions, is chromatin ameno-precipitation something that is do-able here at CU Boulder? For western bloting, what does it specifically tell you?
Of course it is doable at CU Boulder; however, it might not be available in student labs. Western blotting will tell you about protein expression, specifically confirms the presence of a protein.
You mention that because Dcr2 gene expression was increased in damage cells, that your hypothesis was supported. How could this information be used practically to manage diseases caused by DNA damage?
Great question! Unfortunately this information alone does not help us to manage any type of diseases. Further research is needed. For example, we know that Dcr is a tumor suppressor, but we can’t treat cancer yet because it must be much more complex.
curesymposium.org 
What kinds of suspected applications does Dcr2 gene modification have in industries?
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I am not sure if I really understood your question. I have not done any research regarding gene modification of Dcr2.
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Why exactly does DNA damage cause Dicer 2 to be more highly expressed?
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There could be many reasons. One is Dcr2 is directly involved in DNA damage repair mechanism, so as the damage is induced, the need for Dcr2 increases. Another could be since dicer is an endoribonuclease, it has a role in making miRNAs that are needed for DNA damage response pathway.
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For your future directions, is chromatin ameno-precipitation something that is do-able here at CU Boulder? For western bloting, what does it specifically tell you?
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Of course it is doable at CU Boulder; however, it might not be available in student labs. Western blotting will tell you about protein expression, specifically confirms the presence of a protein.
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You mention that because Dcr2 gene expression was increased in damage cells, that your hypothesis was supported. How could this information be used practically to manage diseases caused by DNA damage?
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Great question! Unfortunately this information alone does not help us to manage any type of diseases. Further research is needed. For example, we know that Dcr is a tumor suppressor, but we can’t treat cancer yet because it must be much more complex.
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Could this research be used outside of just a medical/healthcare setting and how?
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Yes, it can. For example, it can be used in research settings and academia.
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