The Open Gene Therapy Journal (Open Gene Ther J)
The Open Gene Therapy Journal is an Open Access online journal which publishes original research articles in all areas on experimental and clinical gene therapy research. The journal scope includes all aspects of human gene therapy research; viral vectors; gene transfer and expression; gene delivery systems; and animal models. The Open Gene Therapy Journal, a peer reviewed journal, aims to provide the most complete and reliable source of information on current developments in all areas of the field. The emphasis will be on publishing quality articles rapidly and freely available to researchers worldwide.
- WebsiteThe Open Gene Therapy Journal website
Material typeDocument, Internet resource
Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
- Author can archive a pre-print version
- Author cannot archive a post-print version
- 12 months (unless federal, government, funding agencies or local policy mandates for the author's institute a different policy on self-archiving)
- On authors personal or authors institutions server
- Published source must be acknowledged
- Must link to journal home page
- Publisher's version/PDF cannot be used
- Articles in all journals can be made Open Access on payment of additional charge
Publications in this journal
Article: Ceiling culture-derived proliferative adipocytes are a possible delivery vehicle for enzyme replacement therapy in lecithin: cholesterol acyltransferase deficiency[show abstract] [hide abstract]
ABSTRACT: Human proliferative adipocytes propagated via ceiling culture technique from subcutaneous fat tissue (desig-nated as ccdPA) were herein evaluated for their potential as a recipient for retroviral vector-mediated gene transduction of a therapeutic protein delivery. Exposure to the ZsGreen-expressing vector supernatant using a cell preparation generated by a 7-day ceiling culture induced a 40-50% transduction efficiency, with less than two integrated copies of viral genome per cell on average. The lcat gene-transduced human ccdPA secreted functional LCAT protein, correlating with the inte-grated copy number of vector genome. The gene-transduced cells could be expanded up to nearly 10 12 cells from 1 g of fat tissue within one month after fat tissue preparation. The cells also maintained the potential to differentiate into adipocytes in vitro. The presence of human LCAT protein in serum was immunologically identified upon transplantation of lcat-expressing ccdPA into the adipose tissue of immune-deficient mice. These results indicated that human ccdPA has a novel therapeutic potential for LCAT-deficient patients. The clinical application in combination with cell transplantation shed a light on a development of a life-long protein replacement therapy for LCAT-deficient patients.The Open Gene Therapy Journal 01/2011; 4.
[show abstract] [hide abstract]
ABSTRACT: Adenovirus release is not triggered until late times after viral infection, when the adenovirus death protein (ADP) accumulates to induce viral egress. Thus, the natural rate of adenovirus release may hinder the spread of oncolytic adenoviruses. Several experimental approaches have provided evidence indicating that promoting adenovirus release can be used to enhance their therapeutic potential. This review briefly summarizes what is known about the mechanism of adenovirus release and describes three different strategies, ADP overexpression, apoptosis induction, and bioselection, which can be used to enhance adenovirus release. Finally we will discuss some of the future perspectives that will contribute to the better use of progeny release for the improvement of the antitumor activity of oncolytic adenoviruses.The Open Gene Therapy Journal 01/2010; 3:24-30.
Article: Enhanced Gene Delivery to Human Primary Endothelial Cells Using Tropism-Modified Adenovirus Vectors.[show abstract] [hide abstract]
ABSTRACT: Endothelial cells have been noted to have relatively low expression of the native receptor for adenovirus serotype 5 (Ad5), coxsackie and adenovirus receptor (CAR), and are thus refractory to Ad5 infection. In this study, we hypothesize that increases in the infectivity of Ad5 in primary human pulmonary artery (HPAEC), coronary artery (HCAEC) and umbilical vein endothelial cells (HUVEC) can be achieved through genetic capsid modification of Ad5 to bypass CAR-dependent infection. The modifications tested in this study include incorporation of an integrin-binding RGD peptide motif (Ad5.RGD), a poly-lysine motif (Ad5.pK7), a combination of both of these peptide domains (Ad5.RGD.pK7), an adenovirus serotype 3 knob domain (Ad5/3Luc1) and canine adenovirus serotype 1 or 2 knob domains (Ad5Luc1-CK1 and Ad5Luc1-CK2). In HPAEC and HCAEC, the greatest infectivity enhancements were achieved using Ad5/3Luc1 (26-fold and 30-fold respectively). HUVEC was most readily infected by Ad5Luc1-CK1 (213-fold). These results demonstrate that gains in Ad5 infectivity in endothelial cells can be accomplished with genetic capsid modifications.The Open Gene Therapy Journal 01/2008; 1:7-11.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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