Association of the pr peptides with dengue virus at acidic pH blocks membrane fusion. Reciprocal effects of fibroblast growth factor receptor signaling on dengue virus replication and virion production. Characterization of class I and II ADP-ribosylation factors (Arfs) in live cells: GDP-bound class II Arfs associate with the ER-Golgi intermediate compartment independently of GBF1. Ciliary targeting motif VxPx directs assembly of a trafficking module through Arf4. Isoform-selective effects of the depletion of ADP-ribosylation factors 1-5 on membrane traffic. Class II ADP-ribosylation factors are required for efficient secretion of dengue viruses. ARF family G proteins and their regulators: roles in membrane transport, development and disease. A scalable strategy for high-throughput GFP tagging of endogenous human proteins. D., Sekine, S., Kamiyama, D., Weissman, J. Sensory-neuropathy-causing mutations in AT元 cause aberrant ER membrane tethering. Atlastins remodel the endoplasmic reticulum for selective autophagy. Efficient protein targeting to the inner nuclear membrane requires Atlastin-dependent maintenance of ER topology. Pawar, S., Ungricht, R., Tiefenboeck, P., Leroux, J. Rab proteins of the endoplasmic reticulum: functions and interactors. A conserved role for atlastin GTPases in regulating lipid droplet size. Human atlastin GTPases mediate differentiated fusion of endoplasmic reticulum membranes. A disease causing ATLASTIN 3 mutation affects multiple endoplasmic reticulum-related pathways. Mutations in a newly identified GTPase gene cause autosomal dominant hereditary spastic paraplegia. Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3. A novel missense mutation confirms AT元 as a gene for hereditary sensory neuropathy type 1. Hereditary spastic paraplegia: clinical features and pathogenetic mechanisms. Mammalian knock out cells reveal prominent roles for atlastin GTPases in ER network morphology. Atlastin GTPases are required for Golgi apparatus and ER morphogenesis. Rismanchi, N., Soderblom, C., Stadler, J., Zhu, P. Homotypic fusion of ER membranes requires the dynamin-like GTPase atlastin. A class of dynamin-like GTPases involved in the generation of the tubular ER network. Shaping the endoplasmic reticulum into a social network. Fusion of the endoplasmic reticulum by membrane-bound GTPases. Cooperation of the ER-shaping proteins atlastin, lunapark, and reticulons to generate a tubular membrane network. Reconstitution of the tubular endoplasmic reticulum network with purified components. Untangling the web: mechanisms underlying ER network formation. The endoplasmic reticulum provides the membrane platform for biogenesis of the flavivirus replication complex. Composition and three-dimensional architecture of the dengue virus replication and assembly sites. Ultrastructural characterization of zika virus replication factories. Rewiring cellular networks by members of the Flaviviridae family. Zika virus: history of a newly emerging arbovirus. Dengue vaccine: WHO position paper, July 2016 - recommendations. Our data identify ATLs as central hubs targeted by flaviviruses to establish their replication organelle and to achieve efficient virion maturation and secretion. Screen analysis confirmed non-redundant ATL functions and identified a specific role for AT元, and its interactor ARF4, in vesicle trafficking and virion maturation. We characterized non-conserved functional domains in ATL paralogues and show that the ATL interactome is profoundly reprogrammed following dengue virus infection. Here, we show that atlastins (ATLs), a subset of ER resident proteins involved in neurodegenerative diseases, have dichotomous effects on flaviviruses-with ATL2 depletion leading to replication organelle defects, and AT元 depletion to changes in virus production pathways. However, it remains unclear how these membranes and associated cellular proteins act during the virus cycle. Flaviviruses, including dengue virus and Zika virus, extensively remodel the cellular endomembrane network to generate replication organelles that promote viral genome replication and virus production.
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