charge reversal
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2022 ◽  
Vol 20 (1) ◽  
Author(s):  
Peng Zhang ◽  
Daoyuan Chen ◽  
Lin Li ◽  
Kaoxiang Sun

AbstractSurface charge of biological and medical nanocarriers has been demonstrated to play an important role in cellular uptake. Owing to the unique physicochemical properties, charge-reversal delivery strategy has rapidly developed as a promising approach for drug delivery application, especially for cancer treatment. Charge-reversal nanocarriers are neutral/negatively charged at physiological conditions while could be triggered to positively charged by specific stimuli (i.e., pH, redox, ROS, enzyme, light or temperature) to achieve the prolonged blood circulation and enhanced tumor cellular uptake, thus to potentiate the antitumor effects of delivered therapeutic agents. In this review, we comprehensively summarized the recent advances of charge-reversal nanocarriers, including: (i) the effect of surface charge on cellular uptake; (ii) charge-conversion mechanisms responding to several specific stimuli; (iii) relation between the chemical structure and charge reversal activity; and (iv) polymeric materials that are commonly applied in the charge-reversal delivery systems. Graphical Abstract


Author(s):  
Christoph Federer ◽  
Victor Claus ◽  
Nathalie Hock ◽  
Julian David Friedl ◽  
Richard Wibel ◽  
...  

2021 ◽  
Vol 221 (2) ◽  
Author(s):  
Daniel Crosby ◽  
Melissa R. Mikolaj ◽  
Sarah B. Nyenhuis ◽  
Samantha Bryce ◽  
Jenny E. Hinshaw ◽  
...  

ER network formation depends on membrane fusion by the atlastin (ATL) GTPase. In humans, three paralogs are differentially expressed with divergent N- and C-terminal extensions, but their respective roles remain unknown. This is partly because, unlike Drosophila ATL, the fusion activity of human ATLs has not been reconstituted. Here, we report successful reconstitution of fusion activity by the human ATLs. Unexpectedly, the major splice isoforms of ATL1 and ATL2 are each autoinhibited, albeit to differing degrees. For the more strongly inhibited ATL2, autoinhibition mapped to a C-terminal α-helix is predicted to be continuous with an amphipathic helix required for fusion. Charge reversal of residues in the inhibitory domain strongly activated its fusion activity, and overexpression of this disinhibited version caused ER collapse. Neurons express an ATL2 splice isoform whose sequence differs in the inhibitory domain, and this form showed full fusion activity. These findings reveal autoinhibition and alternate splicing as regulators of atlastin-mediated ER fusion.


Author(s):  
Jingyi Liu ◽  
Zhoutong Dai ◽  
Yu Zhou ◽  
Wangwang Tao ◽  
Hongxiang Chen ◽  
...  

2021 ◽  
pp. 2100560
Author(s):  
Jaeyu Lee ◽  
Seongjun Moon ◽  
Yong Bin Han ◽  
Seung Jae Yang ◽  
Joerg Lahann ◽  
...  

2021 ◽  
Vol 338 ◽  
pp. 719-730
Author(s):  
Zimu Li ◽  
Yao Yang ◽  
Huaxuan Wei ◽  
Xiaoting Shan ◽  
Xuanzhi Wang ◽  
...  
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