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These results add to the growing evidence that suggests that macrophages are a major source of VEGFC in pathological tissues and, therefore, function as central regulators of the lymphatic vascular surface area [ 54, 55].
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In particular, three TNF family molecules - the receptor activator of NF-κB, its ligand RANKL, and the decoy receptor of RANKL, osteoprotegerin - have established their pivotal role as central regulators of osteoclast development and osteoclast function [ 29].
The transcriptional regulator σB functions as central regulator of general stress responses in Gram-positive bacteria with a low GC content including the genera Bacillus, Staphylococcus and Listeria with variations in regulon-members and -size [19], [23], [24], [30] [35].
Furthermore, macrophages have been identified as central regulators of HSC egress from the BM after phagocytosis of aged neutrophils.
KNOXI proteins emerge as central regulators of hormone levels in plant meristems.
Cellular mechanical properties have emerged as central regulators of many critical cell behaviors, including proliferation, motility, and differentiation.
Ror proteins have emerged as central regulators of Wnt signaling [1].
Rab ("Ras-related in brain") GTPases have emerged as central regulators of vesicle budding, motility, and fusion.
Cytoplasmic PABPs are conserved across eukaryotes and are best characterized as central regulators of mRNA translation (reviewed in [ 6– 8]).
We therefore characterized these central regulators of the cytoskeleton as potential interactors of LRRK2.
The prototypical cytoplasmic member, PABP1, is a multifunctional RNA-binding protein with roles in global and mRNA-specific translation and stability, consistent with a function as a central regulator of mRNA fate in the cytoplasm.
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