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AAA+ proteins: have engine, will work
TLDR
The structural organization of AAA+ proteins, the conformational changes they undergo, the range of different reactions they catalyse, and the diseases associated with their dysfunction are reviewed.
Membrane budding and scission by the ESCRT machinery: it's all in the neck
TLDR
The endosomal sorting complexes required for transport (ESCRTs) catalyse one of the most unusual membrane remodelling events in cell biology, which is crucial for many processes, including the biogenesis of multivesicular bodies, viral budding, cytokinesis and, probably, autophagy.
Calmodulin Trapping by Calcium-Calmodulin-Dependent Protein Kinase
TLDR
The experiments demonstrate the existence of a new state in which calmodulin is bound to CaM kinase even though the concentration of calcium is basal, and provides for molecular potentiation of calcium transients and may enable detection of their frequency.
Plasma membrane deformation by circular arrays of ESCRT-III protein filaments
TLDR
It is suggested that ESCRT-III polymers delineate and help generate the luminal vesicles of multivesicular bodies and form novel membrane-attached filaments that can promote or stabilize negative curvature and outward budding.
Synaptobrevin binding to synaptophysin: a potential mechanism for controlling the exocytotic fusion machine.
TLDR
It is concluded that synaptophysin selectively interacts with synaptobrevin in a complex which excludes the t‐SNAP receptors syntaxin I and SNAP‐25, suggesting a role for synaptophysicalin in the control of exocytosis.
Multivesicular body morphogenesis.
TLDR
Current understanding of the cellular functions of MVBs and how the ESCRT machinery contributes to MVB morphogenesis are summarized and critical areas in which further mechanistic and spatiotemporal studies in living cells will advance this exciting area of research are identified.
The pathophysiological basis of dystonias
TLDR
Dystonia offers a window into the mechanisms whereby subtle changes in neuronal function, particularly in sensorimotor circuits that are associated with motor learning and memory, can corrupt normal coordination and lead to a disabling motor disorder.
Neuronal Ca2+/calmodulin-dependent protein kinases.
TLDR
It is established that this Ca(2+)-independent activity is generated in situ in response to a variety of cell stimuli, and the study of substrates and their functions promises to continue providing exciting insights into the control of cellular signalling by Ca2+.
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