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Past evidence suggests that a principal function of the prefrontal cortex (PFC) is selective attention and that this function involves the modulation of sensory signals within posterior cortices.
Execution of this function involves the enforcement of a VSN at the WSI level.
This function involves TRPV4-dependent calcium entry, with subsequent activation of Rho kinases and actin rearrangement.
This function involves the coordinated activity of ferritin heavy chain (FTH1) and ferritin light chain subunits.
The mechanism of this function involves uPA binding to uPAR and activating plasminogen, which initiates a hydrolysis cascade of related proteins that drives degradation of the extracellular matrix.
The unique pattern of JNK activation and its requirement in mesenchymal progression during EMT prompted us to investigate whether this function involves gene regulatory events.
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It is important to note that although numerous studies have addressed the role of the prefrontal cortex in episodic memory, a number of studies have also demonstrated the involvement of a more distributed neural network sustaining this function involving the temporal lobes and parietal cortices.
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While this distinct function involves interactions with other cellular components (e.g., DnaA), biochemical evidence suggests that differential regulation of ParA dimeric states by ParB also plays an important role.
The pathogenesis of this deterioration of organ function involves oxidative stress caused by reactive oxygen species (ROS) [ 1].
Executive function involves three important skills.
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