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Although the substrate-dependent spin state regulation for some CYPs is well documented, the molecular basis for the variability in the substrate-free ferric spin equilibrium has not been determined.
In summary, all these results support a relatively minor contribution of the phenotypic plasticity to the ecotype differences observed in the proteome expression, suggesting an important genetic basis for the variability in gene expression in this species.
We do not yet understand the basis for the variability, but assume that it represents a transient state and that these large cells begin to divide later than the others.
Monteith et al. (2011b suggested that plasticity in mule deer migration might allow the species to avoid such mismatches; however, if there is a genetic basis for the variability in migration among individuals, there may be less plasticity and more natural selection at work (Nelson 1998).
Our results support a relatively minor contribution of genetic factors to the TYP and LON morphological forms differences observed in the three gene markers, suggesting an important phenotypic plasticity basis for the variability in morphology, life history, and ecology in S. japonica.
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The basis for this variability is unknown, but we observed a similar level of variation in another cell line that has a single copy of an unrelated GFP transgene: Jupiter (Karpova et al. 2006) (data not shown).
RhoB has different effects on cell migration depending on the cell type and conditions, but the molecular basis for this variability is unclear.
The molecular basis for this variability is currently unknown but seems to be independent of the nature of the ABCD1 mutation; therefore the time of onset is unpredictable for pre-symptomatic patients.
Identifying and understanding the neuroendocrine basis for this variability in rats and other species will be important for understanding the evolutionary physiology of reproductive strategies and for understanding genetic variation in brain function.
For instance, it is tempting to hypothesize that the variability in HSF1 and HSF2 levels among individuals and consequently on their ratio could constitute a molecular basis for the enigmatic variability in sensitivity to FAS that is observed in the human population (reviewed in Gressens et al, 2001).
These results may provide a molecular basis for the inherent variability in the response of muscle from older as compared with younger individuals to resistance training.
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