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In particular, microfluidic compartmentalization has been widely utilized.
Tissue compartmentalization has been reported for other sites such as cerebral spinal fluid, brain, the male and female genital tracts, lymphoid cells, blood monocytes, and the lung [23], [24], [25], [26], [27], [28], [29].
Purinergic receptor compartmentalization has been observed in different cells.
Chromosomal compartmentalization has been recognized as important for genome function.
Such compartmentalization has been shown within pancreatic β-cells (18).
The physiology of the joint compartment differs from the periphery, and Treg compartmentalization has been shown to be tissue- and organ-specific [ 17, 27].
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This suggests that other mechanisms specify epigenetic patterns the underlying DNA sequence and 3D chromosome compartmentalization have been suggested.
Predictions based on simulations of the basal in silico model indicate that only a very small fraction of the PDEs is enzymatically active under basal conditions which might be a result of PDE compartmentalization as has been reported for adipocytes (PDE3), HEK293 cells and cardiac myocytes (PDE4) and platelets (PDE5) [ 20- 22, 45].
Compartmentalization of strains has been reported in transplant recipients [3], in HIV populations [18], [19], and a small series of women with STDs [20].
Targeting and compartmentalization of PKA has been mostly thought to be mediated by A-kinase-anchoring proteins (AKAPs) that bind the dimerization/docking domain of the regulatory subunits and scaffold PKA to substrates [4], [5], [6], [7], [8], [9].
In cultured human IECs, apical versus basolateral compartmentalization of TLR9 has been linked to the distinct immune responses elicited by ligand-activated TLR9 receptors (Lee et al, 2006).
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