Tests for association between genotypes and quantitative traits were performed using Kruskal Wallis analysis of ranks for traits with non-normal distributions, or alternatively, anova for normally distributed traits.
Alternatively, HPTCs, which normally do not express BMP-7, could be genetically engineered to achieve BMP-7 secretion.
Alternatively, transposable elements, which normally are silenced by small RNA pathways in the male and female germ lines, could be de-repressed by the presence of PSR to disrupt the chromatin state of the paternal set (Michalak 2009).
Alternatively, in contrast to normally structured Bcl-2 which forms low conductance channels to maintain physiological mitochondrial Δψ (33, 39), conformationally altered Bcl-2 may change its channel activity and dysregulate mitochondria bioenergetics ultimately causing Cytochrome C release.
Theoretically, the expression of normally and alternatively spliced mutant transcripts which was reflected by the total amount of PCR amplicon of exons 12/13 should be similar or close to the expression of the total TPO transcripts that was represented by the amplicon of exons 4/5.
However, the source of the TPO protein remained unclear since similar size protein can be translated from both normally spliced and alternatively spliced TPO transcripts.
Alternatively, it is conceivable that normally, cohesion is established by cohesin complexes that are loaded de novo onto chromatin during DNA replication.
Alternatively, although HuD is not normally expressed in mature oligodendrocytes, the αCaMKII promoter used here to express transgenic HuD was shown to be active in oligodendrocyte precursor cells (Mason et al., 2003).
Alternatively, 20% of neurons that normally exhibit axon branching phenotypes may be operating using a branching mechanism independent of O-GlcNAc regulation and thus unresponsive to increases in O-GlcNAc levels.
The increase in expression after treatment with 5-Aza-dC could be due to the methylation seen in these fragments in the cell lines or alternatively be explained by other normally methylated genes being activated as a result of the treatment which could have an enhancing effect on the transcription of PIK3CD and CASZ1.
