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The study of cognitive endophenotypes enables an investigation of psychological processes that may mediate genetic effects on behavioural traits or disorders.
Therefore examination of the effect of recently identified risk genes on cognition may prove fruitful in delineating cognitive processes, and by inference neural systems, that may mediate genetic risk.
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In the current manuscript, we utilized computational and bioinformatics approaches to identify regulatory mechanisms that may mediate the genetic response to iron deprivation.
In humans, such penetrance modifiers may mediate expression of genetic diseases arising from loss-of-function mutations (Abecasis et al., 2010; Hamilton and Yu, 2012; MacArthur et al., 2012), and if their crypsis is environmentally influenced they may also explain modern disease susceptibility (Gibson, 2009).
For many years dysfunction of mitochondria has been implicated in OA aetiology and there is some evidence that polymorphism of mitochondrial DNA may mediate this, although the genetic studies so far performed have been on relatively small cohorts (reviewed in Ref. 27).
Recently, it has been demonstrated that MVs may mediate the horizontal transfer of genetic information.
Furthermore, we suggest genetic mechanisms that may mediate any sex bias and three candidate sex-linked genes are considered.
Third, we should bear in mind that dopaminergic neurotransmission may mediate the effect of entirely different genetic variants on exercise behavior, in the absence of a direct effect of dopaminergic genes.
Although it is not known if any of these elements have significant functional roles, the mini-ISs could be responsible for the alteration of the expression of some genes, and they may mediate HGT, thereby contributing to the genetic diversity among H. bizzozeronii strains.
Thus, AbSV may be a vehicle mediating genetic transfer between hosts and other organisms.
Our results suggest that epigenetic processes may mediate previously identified, but as yet unexplained, genetic influences too.
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