Molecular mechanisms of cellular transformation by HTLV-1 Tax

Grassmann, Ralph; Aboud, Mordechai; Jeang, Kuan‐Teh

doi:10.1038/sj.onc.1208978

Cited by 358 publications

(375 citation statements)

References 161 publications

(133 reference statements)

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“…In HTLV-1-expressing cells, the virus-encoded transforming protein, Tax, plays a critical role in the growth and survival of infected T cells by perturbing normal regulatory mechanisms, resulting in uncontrolled cell growth. 18 Tax activates many cellular transcription factors including nuclear factor-jB (NF-jB). 18 NF-jB is a key transcription factor involved in the expression of genes that play key roles in growth, apoptosis and tumorigenesis of many human cancer cells including HTLV-1-infected T cells.…”

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confidence: 99%

“…18 Tax activates many cellular transcription factors including nuclear factor-jB (NF-jB). 18 NF-jB is a key transcription factor involved in the expression of genes that play key roles in growth, apoptosis and tumorigenesis of many human cancer cells including HTLV-1-infected T cells. 19,20 The classical pathway of NF-jB activation involves the IjB kinase (IKK) complex [IKKa, IKKb and IKKg (NEMO)] responsible for phosphorylation of IjB.…”

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confidence: 99%

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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

Intl Journal of Cancer

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Retraction: The following article has been retracted through agreement between the first author and several coauthors, the journal Editor‐in‐Chief, Peter Lichter, and John Wiley & Sons, Ltd.: Tomita M, Toyota M,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.

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confidence: 99%

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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

Intl Journal of Cancer

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“…HTLV-I Tax interacts with and inhibits functions of Chk1/Chk2 (Haoudi et al, 2003;Park et al, 2004Park et al, , 2006. It is well established that HTLV-I Tax oncoprotein inhibits the function of the tumor suppressor p53 protein, although the mechanism of p53 inactivation in HTLV-I biology is still debated (Grassmann et al, 2005). MDMX binds to and inhibits p53 transcriptional activity (Shvarts et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Telomere attrition induces a DNA double-strand break damage signal that reactivates p53 transcription in HTLV-I leukemic cells

Datta

Nicot

2007

Oncogene

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Persistent inhibition of telomerase induces a severe telomere shortening in human T-cell leukemia virus type-1-infected cells which signals a DNA double-strand break damage response, formation of telomere dysfunction-induced foci and activates the ATM pathway. In turn, activation of ATM and its downstream effectors led to an increased phosphorylation and acetylation on specific residues of p53 known to be involved in transcriptional activation. Disruption of Mdm2-p53 complexes coupled with increased proteasomal degradation of MDMX further enhanced reactivation of p53 transcription, ultimately leading to senescence of tumor cells. Induction of senescence in these T-cells was associated with an increased expression of p21, p16 and activation of GSK3b. Our results support the cancer-aging model and demonstrate that the halt of aging in cancer cells can be reversed through reactivation of p53.

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“…The most frequent modifications are N-glycosilation, N-myristylation, and phosphorylation by protein kinases (Adachi et al 1992, Reitter et al 1998, Ono et al 2000, Bouamir et al 2003, Grassmann et al 2005 The HIV-1 epidemic in Brazil was initially dominated by HIV-1 subtype B ) and the virus spread to all the states in the country through different transmission routes. HIV-1 subtype F1 was first identified in Salvador and recombinants of subtypes B and F1 were identified in Rio de Janeiro .…”

Section: The Analysis Of Genetic Data For Human Immunodeficiency Virumentioning

confidence: 99%

Re-mapping the molecular features of the human immunodeficiency virus type 1 and human T-cell lymphotropic virus type 1 Brazilian sequences using a bioinformatics unit established in Salvador, Bahia, Brazil, to give support to the viral epidemiology studies

Queiroz

Mota-Miranda

Oliveira

et al. 2007

Mem. Inst. Oswaldo Cruz

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The analysis of genetic data for human immunodeficiency virus type 1 (HIV-1) and human T-cell lymphotropic virus type 1 (HTLV-1) is essential to improve treatment and public health strategies as well as toRecent advances have led to an unprecedented increase in sequence data for human immunodeficiency virus type 1 (HIV-1) and human T-cell lymphotropic virus type 1 (HTLV-1). For example, the number of HIV-1 sequences in GenBank had increased from approximately 42,000 in September 2000 (Gaschen et al. 2001) to nearly 115,000 sequences on September 2004. These sequences are also a valuable source of data for genetic analyses, such as the HIV-1 drug resistance study in which mutations into protease and reverse transcriptase genes can be used to better manage antiretroviral treatment (Shafer et al. 2000). Vaccine initiatives use sequences from the immunodominant regions of the viruses to design artificial peptides that stimulate the immune system and control the viral replication (Addo et al. 2001). Other research projects are evaluating whether the HTLV-1 envelope protein immunodominant region could elicit neutralizing antibody responses against HTLV-1. Such information could be used in the development of vaccines and to improve diagnostic methods (Sundaram et al. 2004).The post-translational modifications in the virus proteins are essential for HIV-1 and HTLV-1 fitness, assembly, and immune escape. The most frequent modifications are N-glycosilation, N-myristylation, and phosphorylation by protein kinases (Adachi et al. 1992, Reitter et al. 1998, Ono et al. 2000, Bouamir et al. 2003, Grassmann et al. 2005 The HIV-1 epidemic in Brazil was initially dominated by HIV-1 subtype B ) and the virus spread to all the states in the country through different transmission routes. HIV-1 subtype F1 was first identified in Salvador and recombinants of subtypes B and F1 were identified in Rio de Janeiro . A more recent heterosexual epidemic, characterized by the presence of subtype C viruses, was identified in South Brazil , Soares et al. 2003. Other reports have also demonstrated that distinct HIV-1 subtypes (A, B, C, D, F1) and recombinant forms (B/C, B/ F1) are actively participating in the Brazilian Aids epidemic (Morgado et al. 1998, Caride et al. 2001, Soares et al. 2005, Couto-Fernandez et al. 2005, Barreto et al. 2006, De Sa Filho et al. 2006).Financial support: Fapesp, PN-DST/AIDS +Corresponding author: lalcan@cpqgm.fiocruz.br ATLQ and ACAM-M contribute equally to this paper.

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Molecular mechanisms of cellular transformation by HTLV-1 Tax

Cited by 358 publications

References 161 publications

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

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

Telomere attrition induces a DNA double-strand break damage signal that reactivates p53 transcription in HTLV-I leukemic cells

Re-mapping the molecular features of the human immunodeficiency virus type 1 and human T-cell lymphotropic virus type 1 Brazilian sequences using a bioinformatics unit established in Salvador, Bahia, Brazil, to give support to the viral epidemiology studies

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