Key result
Glycosylation of the CAR D2 domain is required for cooperative adenovirus binding, but its absence paradoxically increases adenovirus infection despite decreasing viral binding.
Population
COS-7 and CAR-deficient CHO-K1 cell lines
Comparison
Expression of glycosylation-deficient… vs Expression of wild-type CAR or green fluorescent…
Design
Preclinical
Authors
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Hypothesis-generating for CAR-targeted adenovirus vectors; leaves open net effects on in vivo tropism and efficacy.
p-value: p=<0.01
CAR glycosylation is essential for homophilic cell adhesion, and while D2 domain glycosylation is required for cooperative adenovirus binding, its absence paradoxically enhances viral infection.
Excoffon et al. (2007) studied Adenovirus infection. Site-directed mutagenesis of CAR glycosylation sites vs. Wild-type CAR was evaluated on Adenovirus infection and CAR-mediated cell adhesion (p=<0.01). Glycosylation of the CAR D2 domain is required for cooperative adenovirus binding, but its absence paradoxically increases adenovirus infection despite decreasing viral binding.
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