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Numerous clinical and epidemiological features of BD can be explained by epigenetic misregulation.
This finding might be explained by epigenetic silencing of ABCB1 in OVCAR-4, preventing expression despite reduced levels of its inhibitor DNAJC15.
This differentiation-potential switch could be explained by epigenetic changes, since the promoters of astrocyte-specific marker genes, glial fibrillary acidic protein (Gfap) and S100β, have been shown to become demethylated in late-stage NPCs prior to the onset of astrocyte differentiation; however, whether demethylation occurs generally in other astrocyctic genes remains unknown.
Moreover, the initiation of biological perturbations resulting in malignancy by certain chemical compounds can be explained by epigenetic mechanisms (Stein, 2012).
It has been suggested by others that 'missing heritability', not fully accounted for by conventional genetics, may be explained by epigenetic mechanisms.
This phenomenon could be explained by epigenetic mechanisms, that have been, in fact, involved in the regulation of these miRNAs [ 35, 36].
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However, the degree of phenotypic variability that is explained by epigenetic processes still remains unclear.
Despite this, the magnitude of the phenotypic variation that is explained by epigenetic processes still remains unclear (Grossniklaus et al. 2013; Heard and Martienssen 2014).
This discrepancy between in vitro and in vivo criteria of PSCs for VSELs has recently been explained by epigenetic changes in expression of some paternally imprinted genes [ 67, 72].
Although some diseases associated with dysregulation of epigenetic modification at some genomic region have been found, EWAS has similar drawbacks to GWAS: it is difficult to estimate how much variation in phenotypes, especially for complex traits, is explained by epigenetic polymorphisms, even if there is evidence that they contribute to phenotypes, either biologically or statistically.
Many unresolved X-Files cases that might be accounted for by a genetic mutation could just as easily be explained by an epigenetic modification of the same gene.
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