Over expression of the selectable marker blasticidin S deaminase gene is toxic to human keratinocytes and murine BALB/MK cells

Over expression of the selectable marker blasticidin S deaminase gene is toxic to human keratinocytes and murine BALB/MK cells

Autor Bento, Fernanda Mara Autor UNIFESP Google Scholar
Takeshita, Daniela Autor UNIFESP Google Scholar
Sacramento, Chester Bittencourt Autor UNIFESP Google Scholar
Machado, Tamara Rocha Autor UNIFESP Google Scholar
Mathor, Monica Beatriz Google Scholar
Carmona, Adriana Karaoglanovic Autor UNIFESP Google Scholar
Han, Sang Won Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
IPEN CNEN SP
Resumo Background: the blasticidin S resistance gene (bsr) is a selectable marker used for gene transfer experiments. the bsr gene encodes for blasticidin S (BS) deaminase, which has a specific activity upon BS. Therefore, its expression is supposed to be harmless in cells. the work reported on herein consisted of experiments to verify a possible toxicity of bsr on mammalian cells, which include several cell lines and primary cultures.Results: Murine keratinocyte BALB/MK and human primary keratinocyte cells transduced with the retroviral vector LBmSN, which has an improved expression system of bsr, namely bsrm, died in five days after the transduction. Meanwhile the control vector LBSN, which expresses bsr, did not provoke cell death. the lethal activity of bsrm was observed only in human keratinocytes and BALB/MK cells among the cell types tested here. Death appears to be mediated by a factor, which is secreted by the BALB/MK transduced cells.Conclusion: By our study we demonstrated that the expression of bsrm gene is toxic to human keratinocytes and BALB/MK cells. It is likely over expression of BS deaminase gene is responsible for the death.
Idioma Inglês
Data de publicação 2004-12-02
Publicado em Bmc Biotechnology. London: Biomed Central Ltd, v. 4, 10 p., 2004.
ISSN 1472-6750 (Sherpa/Romeo, fator de impacto)
Publicador Biomed Central Ltd
Extensão 10
Fonte http://dx.doi.org/10.1186/1472-6750-4-29
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000226287100001
Endereço permanente http://repositorio.unifesp.br/handle/11600/28048

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