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Recent studies of human genetic syndromes and transgenic mouse models with vascular pathology have exposed a crucial function of extracellular control in the regulation of TGFβ bioavailability in the vascular system. This Review discusses such regulation and the implications of defects in this process with regards to human health.
Mitochondria constantly fuse and divide, are actively transported to specific subcellular localizations and have dynamic structures. Mitochondrial dynamics is important for the functional state of mitochondria, and defects can manifest in mammalian development, apoptosis and neurodegenerative disease.
Cilia — tiny hair-like organelles attached to the cell surface — are located on most polarized cells and have been adapted as versatile tools for various cellular functions. Several molecular mechanisms affecting the structure and function of distinct cilia types are associated with cilia-related disorders.
The successful completion of mitosis requires that late mitotic events occur in a strict sequence. This is regulated, at least in part, by the order in which different cyclin-dependent kinase substrates are dephosphorylated and in which anaphase-promoting complex substrates are degraded.
Phosphorylation is a universal regulatory mechanism that induces changes in protein conformation. However, certain phosphorylated motifs can be further regulated by the prolyl isomerase PIN1, which is of increasing importance in aspects of physiology and disease.
The vacuolar ATPases are proton pumps that have a central role in maintaining the pH of intracellular compartments and in proton transport across the plasma membrane. Their activity is controlled at many different levels and, increasingly, their dysregulation is being linked to specific diseases.
Ten years ago, few people had heard of the term autophagy (literally 'self-eating'). But less than a decade later, research in the field has exploded, and recent studies have uncovered an integral role for autophagy in various human diseases.
