Positive and negative regulation of adenovirus infection by CAR-like soluble protein, CLSP

Kono, Kenji; Tashiro, Kentaro; Sakurai, Fuminori; Osada, Naoki; Kusuda, Jun; Hayakawa, Tetsuo; Yamanishi, Koichi; Mizuguchi, Hiroyuki

doi:10.1038/sj.gt.3302975

Cited by 8 publications

(6 citation statements)

References 39 publications

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“…The absence of other receptors, presence of mitigating factors (eg. Homologs of mouse CAR-like soluble protein) (Kawabata et al, 2007), or differences in receptor structure must also be considered. Adenovirus attachment is facilitated by fiber protein interacting with CAR, followed by an interaction of the RGD motif on the penton base with αVβ3 or αVβ5 integrins to allow internalization (Bergelson et al, 1997;Zhang and Bergelson, 2005).…”

Section: Discussionmentioning

confidence: 99%

Characterization of a novel adenovirus isolated from a skunk

et al. 2015

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Adenoviruses are a ubiquitous group of viruses that have been found in a wide range of hosts. A novel adenovirus from a skunk suffering from acute hepatitis was isolated and its DNA genome sequenced. The analysis revealed this virus to be a new member of the genus Mastadenovirus, with a genome of 31,848 bp in length containing 30 genes predicted to encode proteins, and with a G+C content of 49.0%. Global genomic organization indicated SkAdV-1 was similar in organization to bat and canine adenoviruses, and phylogenetic comparison suggested these viruses shared a common ancestor. SkAdV-1 demonstrated an ability to replicate in several mammalian liver cell lines suggesting a potential tropism for this virus.

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Section: Discussionmentioning

confidence: 99%

Characterization of a novel adenovirus isolated from a skunk

et al. 2015

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“…efficiency of viral infection into cells cultured as intact COCs appears to be significantly lower than that into mono-layer cells. In addition, a recent study has shown that a rodent specific gene, Clsp (also known as Gm1123) encoding Carlike soluble protein that might play a role in the anti-viral defense, is expressed in mouse brain and ovary (Kawabata et al, 2007). Although the identity of the cell types expressing CLSP in the ovary is currently not determined, it is possible that mouse granulosa cells are more protected from viral infection by this protein.…”

Section: Discussionmentioning

confidence: 99%

Targeted suppression of Has2 mRNA in mouse cumulus cell–oocyte complexes by adenovirus‐mediated short‐hairpin RNA expression

Sugiura

Eppig

2008

Molecular Reproduction Devel

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RNA interference (RNAi) is an effective tool for studying gene function in oocytes, but no studies have targeted somatic cells of primary cultured cumulus cell-oocyte complexes (COCs). This is probably due to difficulty in introducing RNAi-inducing molecules, such as a short-hairpin RNA (shRNA) gene, into COCs by commonly used transfection reagents. We therefore tested whether a developmental process of intact COCs could be suppressed by adenovirus-mediated shRNA expression. Has2, encoding hyaluronan synthase 2, was selected as the target transcript, because the process of cumulus expansion depends upon expression of Has2 mRNA and this process is easily evaluated in vitro. Intact COCs were infected with replication-incompetent adenoviruses containing an expression sequence of shRNA targeting either Has2 (Has2 shRNA) or a control transcript not expressed in cumulus cells, and the effects on epidermal growth factor (EGF)-stimulated cumulus expansion were determined. Has2 shRNA expression suppressed Has2 mRNA levels in COCs by more than 70%, without affecting expression levels of Ptgs2, Ptx3, Tnfaip6 mRNAs, which are also required for cumulus expansion, or other transcripts not related to expansion. Interestingly, levels of Areg and Ereg mRNAs were decreased in COCs expressing Has2 shRNA when compared with those in controls, while Btc mRNA levels remained unaffected. Furthermore, the degree of cumulus expansion by Has2 shRNA-expressing COCs was significantly less than that of controls. Thus adenovirus-mediated introduction of shRNA produces specific gene silencing and a phenotype in intact COCs, providing proof of principle that this method will be a helpful tool for understanding mechanisms of COC development.

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“…It should be noted, that in some cases the potential therapeutic applications from the transformation inhibition effect may be needed [79], e.g., definite diseases are provoked by the 24 excess gene function noncharacteristic for a normal cell. In this case gene therapy has to be directed onto the suppression of superactive gene by means of constructions which would express into the cells factors capable of interacting with an expression product of an unwanted gene, thereby neutralizing its harmful effect.…”

Section: Effect Of Surfactants On Dna Transformationmentioning

confidence: 99%