Dinh 2011/NOTES/2011-11-9: Difference between revisions
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==Localization of shared aberrant CpGs== | ==Localization of shared aberrant CpGs== | ||
*At first glance, shared aberrant CpGs tend to not be in genic regions and are more likely to be in regulatory regions (DNaseI hypersensitivity and TF binding sequence). | *At first glance, shared aberrant CpGs tend to not be in genic regions and are more likely to be in regulatory regions (DNaseI hypersensitivity and TF binding sequence). | ||
*If shared aberrant CpGs are in regulatory regions then how do they regulate the expression of these genes? Is there a correlation? If it is a weak correlation, could it be possible that multiple regulatory "switches" act on this gene to control it's transcription and degradation? Can we find those? | *If shared aberrant CpGs are in regulatory regions then how do they regulate the expression of these genes? Is there a correlation? If it is a weak correlation, could it be possible that multiple regulatory "switches" act on this gene to control it's transcription and degradation? Can we find those? |
Revision as of 20:11, 11 November 2011
- At first glance, shared aberrant CpGs tend to not be in genic regions and are more likely to be in regulatory regions (DNaseI hypersensitivity and TF binding sequence).
- If shared aberrant CpGs are in regulatory regions then how do they regulate the expression of these genes? Is there a correlation? If it is a weak correlation, could it be possible that multiple regulatory "switches" act on this gene to control it's transcription and degradation? Can we find those?