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We thus hypothesized that the loss-of-function of 5-HT2AR malterthe the correct membrane distribution of HCV receptors or entry factors.
The exit factors in the herd dynamics prevailed over the entry factors, and this was not favourable for herd re-building and maintenance.
It aims to clear the principal criteria of measuring inventive efficiency, and demonstrates the necessity of a pertinent selection for entry factors to define indicators.
Herein, we describe the effects of a set of statins on HCV entry and on HCV key entry factors in vitro.
We speculated that 5-HT2AR maffectect other major HCV receptors or entry factors, but the silencing of 5-HT2AR and its antagonist PBZ did not negatively regulate the expression and transcription of major HCV entry factors in whole cell (Figs. 4A, S3 and S6C).
We also confirmed that the HCV inhibition of PBZ is not side-effected by PBZ-mediated cytotoxicity (Figs. S1A, S1B and S6A), changes in cell proliferation (Fig. S6B), or reduced transcription of known HCV receptors or entry factors (Fig. S6C).
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Notably, CLDN-1 is a HCV entry factor and confers HCVcc and HCVpp entry.
We were able to infect mouse cells expressing human CD81 and occludin (OCLN the minimal set of entry factor factors required for HCV uptake into mouse cells.
Using a chemical biology strategy, we have demonstrated that 5-HT2AR is a HCV entry factor that functions in the late endocytosis stage at or before membrane fusion.
Here we identify serotonin 2A receptor (5-HT2AR) is a HCV entry factor amendable to therapeutic intervention by a chemical biology strategy.
Interestingly, CLDN-1 is the first entry factor shown to confer susceptibility to HCV when ectopically expressed in non-hepatic cells.
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