To better understand the functional difference of the enhancer classes defined based on their histone modification states, we asked if there is a correlation between enhancer histone modification state and expression level of their target genes.
To understand the correlation between histone modifications and transcription, we asked if the occupancies of various histone modifications correlate with gene activity in P. falciparum.
Because PHB undergoes both O-GlcNAc modification and tyrosine phosphorylation, we asked the question whether these modifications occur in neighboring residues and affect each other.
Motivated to test the role of the modification in terminating the primer-binding sequence and thus limiting run-on transcription, we asked how the modification of RNA could be accomplished.
Because mitochondria are key players of cell metabolism, we asked whether modifications of metabolic or environmental conditions could influence the capacity of mitochondria-defective cells to maintain nuclear genome stability.
Next, we asked whether U34 modifications mediate decoding specificity, reasoning that if aberrant U34 modification relaxes the specificity of codon binding, hypomodified tRNAs could compete for binding at near-cognate codons with mismatches at the third position, eliciting translational pausing.
Thus, we asked whether this modification can be due to ubiquitination.
As olfactory and vomeronasal neurons are constantly renewed by peripheral neurogenesis following apoptosis, we asked whether the presynaptic modifications may lead to neurogenesis modifications.
