Traffic

Journal: Traffic

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Wiley-Blackwell

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Publications1 - 8 of 8

HCMV Induces Macropinocytosis for Host Cell Entry in Fibroblasts
Hetzenecker, Stefanie; Helenius, Ari; Krzyzaniak, Magdalena A. (2016)
Traffic
Bulk flow revisited
Thor, Friederike; Gautschi, Matthias; Geiger, Roger; et al. (2009)
Traffic
Principles of Virus Uncoating: Cues and the Snooker Ball
Yamauchi, Yohei; Greber, Urs F. (2016)
Traffic
Viruses are spherical or complex shaped carriers of proteins, nucleic acids and sometimes lipids and sugars. They are metastable and poised for structural changes. These features allow viruses to communicate with host cells during entry, and to release the viral genome, a process known as uncoating. Studies have shown that hundreds of host factors directly or indirectly support this process. The cell provides molecules that promote stepwise virus uncoating, and direct the virus to the site of replication. It acts akin to a snooker player who delivers accurate and timely shots (cues) to the ball (virus) to score. The viruses, on the other hand, trick (snooker) the host, hijack its homeostasis systems, and dampen innate immune responses directed against danger signals. In this review, we discuss how cellular cues, facilitators, and built-in viral mechanisms promote uncoating. Cues come from receptors, enzymes and chemicals that act directly on the virus particle to alter its structure, trafficking and infectivity. Facilitators are defined as host factors that are involved in processes which indirectly enhance entry or uncoating. Unraveling the mechanisms of virus uncoating will continue to enhance understanding of cell functions, and help counteracting infections with chemicals and vaccines.
Tec-Kinase-Mediated Phosphorylation of Fibroblast Growth Factor 2 is Essential for Unconventional Secretion
Ebert, Antje D.; Laussmann, Mareike; Wegehingel, Sabine; et al. (2010)
Traffic
Diatrack particle tracking software: Review of applications and performance evaluation
Vallotton, Pascal; Van Oijen, Antoine M.; Whitchurch, Cynthia B.; et al. (2017)
Traffic
Vaccinia Virus Infection Requires Maturation of Macropinosomes
Rizopoulos, Zaira; Balistreri, Giuseppe; Kilcher, Samuel; et al. (2015)
Traffic
The prototypic poxvirus, vaccinia virus (VACV), occurs in two infectious forms, mature virions (MVs) and extracellular virions (EVs). Both enter HeLa cells by inducing macropinocytic uptake. Using confocal microscopy, live-cell imaging, targeted RNAi screening and perturbants of endosome maturation, we analyzed the properties and maturation pathway of the macropinocytic vacuoles containing VACV MVs in HeLa cells. The vacuoles first acquired markers of early endosomes [Rab5, early endosome antigen 1 and phosphatidylinositol(3)P]. Prior to release of virus cores into the cytoplasm, they contained markers of late endosomes and lysosomes (Rab7a, lysosome-associated membrane protein 1 and sorting nexin 3). RNAi screening of endocytic cell factors emphasized the importance of late compartments for VACV infection. Follow-up perturbation analysis showed that infection required Rab7a and PIKfyve, confirming that VACV is a late-penetrating virus dependent on macropinosome maturation. VACV EV infection was inhibited by depletion of many of the same factors, indicating that both infectious particle forms share the need for late vacuolar conditions for penetration.
Investigating Endocytic Pathways to the Endoplasmic Reticulum and to the Cytosol Using SNAP-Trap
Geiger, Roger; Luisoni, Stefania; Johnsson, Kai; et al. (2013)
Traffic
Cholera toxin enters cells via an unusual pathway that involves trafficking through endosomes to the endoplasmic reticulum (ER). Whether the toxin induces its own pathway or travels along a physiological retrograde route is not known. To study its trafficking, we labeled cholera toxin B (CTB) or endogenous plasma membrane proteins with a small chemical compound, benzylguanine, which covalently reacts with the protein SNAP‐tag. Using ER‐targeted SNAP‐tag as reporter, we found that transport of CTB to the ER depends on dynamin‐2 and syntaxin 5. Plasma membrane proteins and a fluid‐phase marker added to the medium were also transported to the ER. This flux was not affected by exposing cells to CTB but was inhibited by depleting syntaxin 5 and increased by depleting dynamin‐2. As a control for confined intracellular localization of ER‐targeted SNAP‐tag we used adenovirus‐5, which traffics to endosomes and then escapes into the cytosol. The virus did not react with ER‐targeted SNAP but with cytosolic SNAP. Together, our results establish a new method (SNAP‐trap) to study trafficking of different cargo to the ER and the cytosol and provide evidence for the existence of a constitutive pathway from the cell surface to the ER.
Five Questions (with their Answers) on ER-Associated Degradation
Brambilla Pisoni, Giorgia; Molinari, Maurizio (2016)
Traffic
Production of a functional proteome is a major burden for our cells. Native proteins operate inside and outside the cells to eventually warrant life and adaptation to metabolic and environmental changes, there is no doubt that production and inappropriate handling of misfolded proteins may cause severe disease states. This review focuses on protein destruction, which is, paradoxically, a crucial event for cell and organism survival. It regulates the physiological turnover of proteins and the clearance of faulty biosynthetic products. It mainly relies on the intervention of two catabolic machineries, the ubiquitin proteasome system and the (auto)lysosomal system. Here, we have selected five questions dealing with how, why and when proteins produced in the mammalian endoplasmic reticulum are eventually selected for destruction.

Publications1 - 8 of 8

Journal: Traffic

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