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Furthermore, being purified and analyzed in vitro, some of these proteins show high aggregation potential and the ability to undergo liquid-liquid demixing, leading to the formation of phase-separated droplets or polymer hydrogels. Cell Motil Cytoskeleton. In order to appropriately balance sources of energy at critical times in development and in response to nutrient stress, a cell can utilize a self-degradative process known as autophagy self-eating that is responsible for the disposal of various intracellular species. Characterization of movement disorder phenomenology in genetically proven, familial frontotemporal lobar degeneration: A systematic review and meta-analysis. What a waste of such a fine actor, who has done much better in Kieslowski's Red? Dual vulnerability of TDP to calpain and caspase-3 proteolysis after neurotoxic conditions and traumatic brain injury. Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: A cross-sectional study. In particular, DERL1 is crucial for the elimination of misfolded proteins from the endoplasmic reticulum.

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    Local functions for FMRP in axon growth cone motility and activity-dependent regulation of filopodia and spine synapses. Mol Cell Neurosci. ALS: A disease of motor neurons and their nonneuronal neighbors. The Cajal body and histone locus body. P-bodies and stress granules: Possible roles in the control of translation and mRNA degradation.

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    Mechanism of cell cycle entry mediated by the intrinsically disordered protein p27 Kip1.

    Obviously, any member of the inducible or modified proteoform i.

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    Tight regulation of unstructured proteins: From transcript synthesis to protein degradation. Local RNA translation at the synapse and in disease. Macromolecular crowding: Obvious but underappreciated.

    played by Jean Rochefort, that tall, long-faced master of sly intrigue.

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    Active liquid-like behavior of nucleoli determines their size and shape in Xenopus laevis oocytes.

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    Therefore, another pathological mechanism of mutant SOD1 has been linked to abnormal axonal synaptic vesicle transport in motor neurons during the early stages of ALS.

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