Heterogeneity of Antigen Molecules Recognized by Anti‐tax<sub>1</sub> Monoclonal Antibody Lt‐4 in Cell Lines Bearing Human T Cell Leukemia Virus Type I and Related Retroviruses

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Retraction: The following article has been retracted through agreement between the first author and several coauthors, the journal Editor‐in‐Chief, Peter Lichter, and John Wiley & Sons, Ltd.: Tomita M, Toyota M, Ishikawa C, Nakazato T, Okudaira T, Matsuda T, Uchihara JN, Taira N, Ohshiro K, Senba M, Tanaka Y, Ohshima K, Saya H, Tokino T, Mori N. (2009). Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV‐1‐infected T cells through enhanced NF‐kappaB activity. Int J Cancer; 124 (June (11)): 2607‐2615, published online on 12 JAN 2009 in Wiley Online Library (www.onlinelibrary.wiley.com). After an investigation the retraction has been agreed due to inappropriate duplication of images and overlap with other published work.

Section: Antibodiesmentioning

confidence: 99%

Retracted: Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV‐1‐infected T cells through enhanced NF‐κB activity

Tomita

Toyota

Ishikawa

et al. 2009

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“…Samples were subjected to electrophoresis on SDS-polyacrylamide gels followed by transfer to a polyvinylidene difluoride membrane and probing with the following specific antibodies: polyclonal antibody to survivin from Santa Cruz Biotechnology (Santa Cruz, CA), and monoclonal antibodies to Tax (Lt-4) 31 and actin from NeoMarkers (Fremont, CA). The bands were visualized with the enhanced chemiluminescence kit (Amersham Biosciences, Piscataway, NJ).…”

Section: Western Blot Analysismentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

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142

112

Survivin, a unique member of the inhibitor of apoptosis protein family, is overexpressed in many cancers and considered to play an important role in oncogenesis. We previously reported the survivin expression profile in ATL, a CD4-positive T-cell malignancy caused by HTLV-I. HTLV-I Tax is thought to play an important role in immortalization of T cells. We have shown also that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by deprivation of IL-2 and converted its growth from being IL-2 dependent to being IL-2 independent through the NF-kB pathway. In our study, we demonstrate that constitutive expression of survivin was associated with resistance to apoptosis after IL-2 deprivation in Tax-expressing CTLL-2 cells. Transient transfection assays showed that survivin promoter was transactivated by Tax, via the activation of NF-kB. Pharmacological NFkB inhibition resulted in suppression of survivin expression and caused apoptosis of Tax-expressing CTLL-2 cells. Our findings suggest that activated NF-kB signaling contributes directly to malignant progression of ATL by preventing apoptosis, acting through the prosurvival protein survivin. ' 2005 Wiley-Liss, Inc.

“…To detect intracellular HTLV-I antigens, mouse monoclonal antibodies (mAbs), Lt-4 (anti-p40 Tax, mouse IgG3), 34 NOR-1 (anti-p24 and p53 Gag; mouse IgG1), 35 GIN-7 (anti-p19, p28 and p53 Gag; mouse IgG2b) 35 and biotinylated GIN-7 were used.…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

Potential immunogenicity of adult T cell leukemia cells in vivo

Kurihara

Harashima

Hanabuchi

et al. 2004

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