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Decoy expression

RRE decoy CD34+ bone marrow cells Traps Rev and thus inhibits transactivation of HIV-1 gene expression Kohn et al. 1999... [Pg.280]

The osteoprotegerin (OPG), also known as OCIF, TR1, or FDCR-1, is the first soluble protein that belongs to the TNF superfamily (Simonet et al. 1997 Kwon et al. 1998 Yun et al. 1998). Unlike RANK and RANKL, OPG is expressed in high concentrations in a variety of tissues and cellular types such as skin, bones, large arteries, and the gastrointestinal tract (Simonet et al. 1997). In bone, OPG is produced by stromal/OB cells (Hofbauer et al. 1999) and works as a decoy receptor for RANKL, competing with RANK for binding RANKL. Therefore, OPG is a potent inhibitor of the OCS. In vitro, OPG inhibits the differentiation and survival of osteoclast precursors, blocks their activation, and induces their apoptosis (Lacey et al. 1998 Yasuda et al. 1998 Hofbauer et al. [Pg.178]

A similar phenomenon has also been reported in B cells derived from chronic lymphoid leukemia (CLL) patients in which mFas is deficient or defective. Fresh de novo CLL cells, which express low levels of mFas, are resistant to agonistic anti-Fas mAb-mediated apoptosis, while CLL cells that acquire abundant mFas after short-term culture become sensitive (T4) to such induction of apoptosis. This flexibility in production of the isoforms is expected to provide a target for selective molecular therapy of tumors on the basis of manipulating decoy action of sFas. [Pg.119]

Thus, the KOB cells have been demonstrated ex vivo to prevent apoptosis by expression on their surfaces of function-ablating Fas antigen, which lacks the entire death domain. These aberrant Fas molecules probably behave as decoy receptors and interfere with the trimerization of normal Fas in a dominant negative manner, resulting in the impairment of signal transduction. [Pg.131]

Jenkins, M., Keir, M., and McCune, J. M., A membrane-bound Fas decoy receptor expressed by human thymocytes. J. Biol. CherrL 275, 7988—7993 (2000). [Pg.135]

Morishita, R., Higaki, J., Tomita, N. and Ogihara, T. (1998) Application of transcription factor decoy strategy as means of gene therapy and study of gene expression in cardiovascular disease. Circulation Res., 82,1023-1028. [Pg.27]

Tomita, N., Morishita, R., Tomita, S., Gibbons, G. H., Zhang, L., Horiuchi, M., Kaneda, Y., Higaki, J., Ogihara, T. and Dzau, V. J. (2000). Transcription factor decoy for NFkappaB inhibits TNF-alpha-induced cytokine and adhesion molecule expression in vivo. Gene Ther. 7, 1326-1332. [Pg.190]

Sakaue, G., Shimaoka, M., Fukuoka, T., Hiroi, T., Inoue, T., Hashimoto, N., Sakaguchi, T., Sawa, Y., Morishita, R., Kiyono, H., Noguchi, K., and Mashimo, T. (2001). NF-kappa B decoy suppresses cytokine expression and thermal hyperalgesia in a rat neuropathic pain model. [Pg.234]

Kubo, T., Kinjyo, N., Ikezawa, A., et al. 2003. Spl decoy oligodeoxynucleotide decreases angiotensin receptor expression and blood pressure in spontaneously hypertensive rats. Brain Res 992 1-8. [Pg.111]

Gene therapy — PNA has been used to manipulate gene expression in disease models by a variety of techniques including anti-sense, anti-gene, and transcription factor decoy approaches (6). [Pg.126]


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Decoy

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