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Indeed, a growing body of data derived from in vitro models suggests that p53 plays a major regulatory role in cell differentiation.
The results of cellular and in vitro models suggests that the Val variant adversely affects mRNA stability and inhibits efficient mitochondrial import of MnSOD precursors, due to partial arrest of the β-sheet structure during transport across the inner mitochondrial membrane 30, 31.
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Available data obtained by in vitro models suggest that there is a correlation between the sulfate content and antioxidant activity.
In vitro models suggest that induction of immunity is controlled by regulating the presentation of antigen, but little is known about how DCs control antigen presentation in vivo.
The impact of Aβ40 oligomers on AD pathogenesis is unclear although some in vitro models suggest that Aβ42 oligomers are significantly more cytotoxic [37].
In vitro models suggest that it derives from reduced stability of mRNA VEGF.
In vitro models suggest that sequestration of CBP/p300 by E1A has the general effect of repressing transcription by any factor that utilises these acetyltransferases (Gallimore and Turnell, 2001).
Together, these two in vitro models suggest that imprinted loci may be susceptible to differential methylation in response to environmental exposures related to development of HCC.
On the other hand, sometimes very high concentrations used in in vitro models suggest caution in the interpretation of in vitro results and again points to the development of more sensitive models.
Previous studies of tamoxifen resistance using in vitro models suggest translocation of ER from nucleus to membrane, facilitating crosstalk with growth factor receptors and enhancing the non-genomic signaling of the ER.
Recent experimental studies have strongly reinforced this hypothesis and some studies involving in vitro models suggest that αS aggregation can spread by axonal transport into the neurons and by cell-to-cell transfer [ 9].
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