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Changes in the level of BIN1 isoforms have been linked to tumor progression, which can be induced by modulation of the expression levels of splicing factors [32], [33].
This response slowing may be induced by modulation of activity in SMC and rIFC, as stimulation of these areas improved stopping performance by delaying responses [25], [26].
Besides local tumor control, systemic anti-tumor effects should be induced by modulation of cell death pathways.
While short-term changes in synaptic properties can be induced by modulation of pre-existing proteins and/or mRNAs, such as trafficking, modification and local translation, long-term changes require transcriptional control of gene expression.
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For example, van den Pol et al. [18] and Obrietan and van den Pol [19] found that they could be induced by the modulation of neurotransmitter, such as gamma-aminobutyric acid (GABA) and glutamate.
In addition, a number of studies have reported that c-Myc expression is repressed by let-7, that p53 interacts with miR-34, and that growth arrest can be induced by miR-34 through modulation of the E2F pathway in human colon cancer cells [46], [47], [48].
In addition, several new genes were found to be induced by IL-1β in OA chondrocytes and their modulation by EGCG was studied.
The modulation of neural responses in IT, furthermore, might be induced by even arbitrary (as opposed to instructed or learned) biases in the perceptual experience of stimuli.
This suggests that the contrast observed in conventional TEM is induced by a modulation in the Al concentration.
So, the memory-state-dependent PV effect observed in Pt/Nd:STO/In device testify the RS is induced by the bias-induced modulation of Schottky barrier on Pt/Nd:STO interface and not by the formation of conductive filaments.
Concomitantly, a fluctuating size of the MPECs is induced by an osmotic pressure modulation within the microgel.
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