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Here, we conducted further studies to better understand the contribution these genes make to the pathogenesis of schizophrenia and ASD.
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Surprisingly, this correlation was not found for repat4, repat6, and repat7 suggesting that the contribution of these genes to Xentari™ resistance in Xen-R is not as important as the contribution of repat5 and arylphorin, or their effect might be masked by the effect of the latter genes in our analysis.
The contribution of these genes to survival in the presence of LC-uFFAs was tested on agar plates containing linoleic acid.
However, the contribution of these genes to the phenotype is unlikely since they are either not or weakly expressed in adult mouse ventricle.
The TLR pathway should therefore be investigated in more detail before drawing definite conclusions about the contribution of these genes to anti-TNF treatment outcome.
The contribution of these genes to gonad integrity maintenance and functionality is apparently unaltered in the hybrids, suggesting that no abrupt shifts in gene expression occurred as a result of hybridisation.
To investigate the contribution of these genes to cognitive symptoms observed in DM1 patients, we studied the effect of deletion of Six5, Dmpk and Mbnl1 on three separate behavioral tasks designed to test learning and memory, anxiety and motivation.
The contribution of these genes to the pathogenesis of breast cancer is still unclear.
We tested the contribution of these genes to circadian behaviour using various dsRNAi knockdown transgenic flies.
Understanding these functions will be critical to recognizing the contribution of these genes in biological processes involved in hepatic functioning.
The contribution of these genes to baculovirus fitness is not clear and is being experimentally tested in our lab.
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