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Richmond Velazquez posted an update 6 months ago
Rab GTPase is a paralog-rich gene family that controls the maintenance of the eukaryotic cell compartmentalization system. Diverse eukaryotes have varying numbers of Rab paralogs. Currently, little is known about the evolutionary pattern of Rab GTPase in most major eukaryotic ‘supergroups’. Here, we present a comprehensive phylogenetic reconstruction of the Rab GTPase gene family in the eukaryotic ‘supergroup’ Amoebozoa, a diverse lineage represented by unicellular and multicellular organisms. We demonstrate that Amoebozoa conserved 20 of the 23 ancestral Rab GTPases predicted to be present in the last eukaryotic common ancestor and massively expanded several ‘novel’ in-paralogs. Due to these ‘novel’ in-paralogs, the Rab family composition dramatically varies between the members of Amoebozoa; as a consequence, ‘supergroup’-based studies may significantly change our current understanding of the evolution and diversity of this gene family. The high diversity of the Rab GTPase gene family in Amoebozoa makes this ‘supergroup’ a key lineage to study and advance our knowledge of the evolution of Rab in Eukaryotes.Selective autophagy receptors have been implicated in the degradation of cellular constituents of various size and rigidity. However, the identity of protein cargo have largely remained elusive. In our recent study, we combined limited proteolysis-enhanced proximity biotinylation and organelle enrichment with quantitative proteomics to map the inventory of autophagosomes in a manner dependent on six different selective autophagy receptors, namely SQSTM1/p62, NBR1, CALCOCO2/NDP52, OPTN, TAX1BP1 and TOLLIP. Conducting this approach under basal and proteostasis-challenged conditions in mammalian cells led to the identification of various new autophagy substrates of which some were degraded through endosomal microautophagy rather than canonical autophagy dependent on the receptors TOLLIP and SQSTM1, respectively.
Wearing blue-blocking lenses (BBLs) in the evening hours may not be effective in improving sleep quality. Optometrists need to be informed in prescribing BBLs by highlighting the consequences of their wear to the circadian system.
Excessive exposure to artificial light, particularly at short wavelengths, during the evening, may disrupt normal nocturnal melatonin production, which is a natural process of the circadian rhythm and affect sleep quality. Current BBLs have been designed to limit blue-light exposure and may offer a means to minimise disruption to the circadian system. The purpose of this study was to evaluate the impact of BBLs on a normal sleep-wake circadian rhythm.
Seven different commercial brands of BBLs (Crizal Prevencia, Smart Blue Filter, Blu-OLP, Blue Control, UV++Blue Control, SeeCoat Blue UV and Blue Guardian) and powers (+2.00 D, -2.00 D and Plano) were evaluated by quantifying the degree to which they reduce light radiation from lamps and electronic devices. In particular, the non-linear circadian index and the circadian stimulus was determined for various light sources to establish changes in melatonin production that occur while viewing through different BBLs.
A large difference was shown in the effectiveness of different BBL brands in reducing the spectral sensitivity of the circadian system. The BBL brand was shown to selectively affect the non-linear circadian index and circadian stimulus, particularly with those with transmittance profiles that block the most blue light having the lowest effect on the suppression of nocturnal melatonin secretion.
BBLs may not improve sleep quality, because they continue to allow the transmittance of blue light that may suppress nocturnal melatonin secretion and hence disrupt the normal sleep-wake circadian rhythm.
BBLs may not improve sleep quality, because they continue to allow the transmittance of blue light that may suppress nocturnal melatonin secretion and hence disrupt the normal sleep-wake circadian rhythm.Alzheimer disease (AD) is a neurodegenerative disorder for which no approved medication exists. AD is characterized by worsening cognitive and non-cognitive symptoms, and research in the AD field strives to identify very precocious brain alterations leading to an irreversible condition. Recently it has been demonstrated that several early AD symptoms are paralleled with degeneration of neurons producing dopamine (DA), a neurotransmitter involved in the regulation of cognitive and non-cognitive functions. Actually, we found that ventral tegmental area (VTA) DA neurons degenerate early in a validated AD mouse model (Tg2576). Here, we summarize new data showing how macroautophagy/autophagy impairment – due to enhanced activity of the ABL/c-Abl kinase – might cause the DA neuron loss. We also proved that nilotinib, an ABL inhibitor, restores autophagy flux, thus preventing VTA neurodegeneration. Divarasib cell line Most notably, from a clinical point of view, nilotinib, by preventing DA neuronal loss, preserves DA outflow in VTA-projecting areas, improving Tg2576 behavioral phenotypes. Our findings shed light on the mechanism involved in DA neurodegeneration, revealing that autophagy represents a viable therapeutic target in early AD.The gastrointestinal tract is the main ecological niche in which Lactobacillus strains may provide health benefits in mammals. There is currently a need to characterize host-microbe interactions in space and time by tracking these bacteria in vivo. We combined noninvasive whole-body imaging with ex vivo fluorescence confocal microscopy imaging to monitor the impact of intestinal inflammation on the persistence of orally administered Lactobacillus plantarum NCIMB8826 in healthy and inflamed mouse colons. We developed fluorescent L. plantarum strains and demonstrated that mCherry is the best system for in vivo imaging and ex vivo fluorescence confocal microscopy of these bacteria. We also used whole-body imaging to show that this anti-inflammatory, orally administered strain persists for longer and at higher counts in the inflamed colon than in the healthy colon. We confirmed these results by the ex vivo confocal imaging of colons from mice with experimental colitis for 3 days after induction. Moreover, extended orthogonal view projections enabled us to localize individual L.
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