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Using methods described by Karginov and colleagues [33] with some modifications, we found that FAF1 is a putative target of miR-24.
While knockdown of ADNP had no effect on HP1 distribution and heterochromatic histone and DNA modifications, we found ADNP silencing major satellite repeats.
In a simplified analysis of allergens for which three dimensional structure data could be either obtained or calculated, without accounting for post translational modifications, we found a highly significant tendency towards an acidic pI and a negative surface charge compared to non-allergens.
Regarding histone modifications, we found that several subunits of the histone acetyltransferase complex SAGA were required to tolerate the damage generated by cell wall stress, particularly by CR.
For 3' modifications, we found that cellular miRNAs tended to have increased numbers of modified 3' ends with added A residues.
Using the BGS protocol [ 1] in over 400 sequencings, even with some modifications, we found that incomplete cytosine to uracil conversion and DNA degradation formed insurmountable challenges.
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In contrast to DNA methylation and H3K27me3 modification, we found that H3K36me3 modification primarily regulates ASE.
Consistent with programming of epiblast in vivo by H3K9me2 modification, we found genome-wide accumulation of H3K9me2 in primed pluripotent cells.
In addition to identifying YTH domain-containing proteins and ALKBH5, known interactors of this modification, we find that FMR1 and LRPPRC, two proteins associated with human disease, "read" this modification.
Subsequently, a meta-regression was performed using a Knapp-Hartung modification, and we found that differences in geographical region may contribute to the heterogeneity we observed (P = 0.025).
Indeed, it is possible that tRFs may play a role in DNA and chromatin modification because we found that tRFs associated with AGO4, which is known to be involved in this process [ 12].
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