Advertisement
JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1074/jbc.R400009200 on April 16, 2004

J. Biol. Chem., Vol. 279, Issue 31, 31991-31994, July 30, 2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
279/31/31991    most recent
R400009200v1
Right arrow Submit a Letter to Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jeang, K.-T.
Right arrow Articles by Aboud, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jeang, K.-T.
Right arrow Articles by Aboud, M.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Minireview

Life, Death, and Tax: Role of HTLV-I Oncoprotein in Genetic Instability and Cellular Transformation*

Kuan-Teh Jeang{ddagger}§, Chou-zen Giam¶, Franca Majone||, and Mordechai Aboud**

From the {ddagger}Laboratory of Molecular Microbiology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, ||Department of Biology, University of Padua, Padua, Italy, and **Department of Microbiology, Ben-Gurion University, Be'er Sheva 84105, Israel


   INTRODUCTION
TOP
 INTRODUCTION
The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 
Human T-cell leukemia virus type I (HTLV-I)1 causes adult T-cell leukemia (ATL) (1–3). The virus is also associated with a neuropathy/myelopathy termed HTLV-associated myelopathy and tropical spastic paraparesis. ATL develops in 2–5% of HTLV-I-infected individuals after a long latent period, suggesting a multistage process of immortalization and transformation of T-lymphocytes. Extant data suggest that 8 discrete events likely occur serially in vivo before an HTLV-I-infected cell becomes immortalized and transformed (4). How HTLV-I infection progresses from clinical latency to T-cell malignancy is not well understood but involves the unique viral transactivator/oncoprotein, Tax (Fig. 1). Tax has been shown to be singly sufficient for immortalizing T-lymphocytes (5, 6) and transforming rat fibroblasts (7). Further, transgenic mice expressing Tax (driven by the HTLV-I long terminal repeat (LTR)) develop neurofibroma, a tumor of mesenchymal tissue (8). Finally, large granular lymphocytic leukemia has been found in mice transgenic for Tax expressed from the T-cell specific, granzyme B promoter (9).



View larger version (37K):
[in this window]
[in a new window]
  		FIG. 1.
HTLV-I Tax interacts with many cell cycle factors. A, genome organization of HTLV-I with an enlarged presentation of the Tax-encoding pX region. B, a tabular summary of some of the cell cycle factors that have been found to interact with Tax.

 
It is estimated that cells in the human body divide 1016 times during a lifetime. To control and prevent errors in cell divisions, mammalian cells have evolved "gatekeepers" and "caretakers" to regulate the rate of cell growth and the fidelity by which cellular genetic information is transmitted to progenies (10). Gatekeepers monitor the net proliferative capacity of a cell, whereas caretakers act to eliminate DNA damages. Accordingly, one perspective is that transformation occurs when both gatekeeper and caretaker functions are abrogated. Using HTLV-I as a model, we review in a non-exhaustive fashion current thoughts on how Tax perturbs normal cellular regulation and engenders cellular transformation.


   The Molecular Biology of HTLV-I
TOP
 INTRODUCTION
 The Molecular Biology of...
Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 
HTLV-I belongs to the Deltaretrovirus genera of the Orthoretrovirinae family. In vivo, the virus has a tropism for CD4+ T-cells (11) although CD8+ T-cells may also serve as a reservoir (12). HTLV-I infection is primarily transmitted via cell-cell contact (13, 14). Recently, the human Glut1 glucose transporter has been identified as a receptor for infection by cell-free virus (15). The proviral genome of HTLV-I is roughly 9 kbp, and like other retroviruses, contains two LTRs flanking structural genes encoding Gag, Pol, and Env (Fig. 1). An additional region located between env and the 3'-LTR, known as the pX region, encodes accessory proteins. The pX region has four partially overlapping reading frames (ORF, Fig. 1), of which ORF IV encodes Tax.

Tax is predominantly a nuclear phosphoprotein (16), which can shuttle into the cytoplasm using a nuclear export signal (17). The mechanism of this shuttling is unclear; however, recent findings that Tax binds tristetrapolin (18) and that tristetrapolin associates with nucleoporin Nup214 (19) raise the possibility that tristetrapolin may serve as a possible nucleocytoplasmic transporter for Tax. Nevertheless, the primary nuclear activity of Tax is to modulate transcription from the HTLV-I LTR (20–22) and cellular promoters including those for IL-2, IL-13, IL-15, IL-2R, c-Fos, and granulocyte macrophage colony-stimulating factor (23–30) among others. Indeed the breadth of Tax's transcriptional reprogramming of host cell genes was verified by DNA array studies which showed that of 2000 assayed genes the expression profiles of ~300 were significantly altered (31). Tax influences so many promoters through its capacity to act in four discrete signaling pathways: CREB/ATF (reviewed in Ref. 32); NF-{kappa}B (reviewed in Ref. 33); AP-1 (34); and SRF (35). These Tax signaling cascades are discussed in greater detail elsewhere (36).


   Tax and Cell Cycle Progression
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 
In the course of transforming cells, viral oncoproteins such as E1A, HPV E7, and SV40 T Ag profoundly dysregulate cell cycle controls (37–39). Transition from one phase of the cell cycle to the next is normally governed by cyclin-dependent kinases (CDKs) partnered with cyclins. These CDK-cyclin complexes are in turn modulated by phosphorylation mediated through CDK-activating kinases and phosphatases, and through physical sequestration by CDK inhibitory proteins (reviewed in Refs. 40 and 41).

An important cell cycle control resides at the transition from G1 to S, which is substantially governed by the retinoblastoma tumor suppressor (Rb) (42, 43). At this juncture, D- and E-cyclins with partner CDKs (reviewed in Refs. 40, 41, and 44) converge to phosphorylate Rb. Hypophosphorylated Rb sequesters and inactivates E2F factors, which are needed for the expression of genes (such as dihydrofolate reductase, DNA polymerase {alpha}, and cyclins) that are critical for S phase events (reviewed in Ref. 45). Hyperphosphorylated Rb releases E2F, activates E2F-responsive genes, and secures the passage of cells from G1 into S (45–48). Thus, regulation of Rb phosphorylation by cyclin-Cdk and CDK inhibitory proteins such as p16INK4a, p21CIP1/WAF1, and p27Kip1 is a critical mechanism for influencing gatekeeper function (37).

Tax reprograms G1 to S progression through multiple mechanistic ways (i.e. direct protein-protein binding, transcriptional induction/repression, and post-translational modification such as phosphorylation). Fig. 1B summarizes several key cell cycle factors that have been experimentally shown to be influenced by Tax. For instance, Tax can directly bind p16INK4a, CycD2, pro-IL-16, and Cdk4 (49–56). On the other hand, p18INK4c (53, 57), CycA (58), CycC (31), CycD2 (31, 51–55, 60), CycE (51), Cdk2 (51), p21CIP1/WAF1 (53, 54, 59–63), and E2F (64–66) are regulated by Tax via transcriptional induction/repression (see Fig. 1B). Finally, Tax via an unknown mechanism influences the phosphorylation of CycD3 (65). To properly consider this complex pattern of interactions, one should appreciate that the context of Tax's up- or down-regulation matters. An instructive example is presented by Tax-p21CIP1/WAF1 interaction. Various studies agree that p21CIP1/WAF1 levels are significantly elevated in Tax-expressing cells (53, 54, 61–63). However, depending on whether p21CIP1/WAF1 complexes with CycD/Cdk2 or CycA/Cdk2, it has been noted that the resulting ternary complex either promotes or inhibits G1/S progression (67–69). These observations, if correct, help to explain seemingly opposing effects of Tax on CycD (up-regulated (31, 51–55)) and CycA (down-regulated (58)) transcription. Indeed, enhanced transcription of CycD in the face of repressed transcription of CycA would tip the balance toward more G1/S transition-promoting p21CIP1/WAF1/CycD/Cdk2 at the expense of G1/S transition-inhibiting p21CIP1/WAF1/CycA/Cdk2 moieties. To date, collective evidence do support that Tax has evolved diverse means to defuse various cellular brakes that guard against accelerated G1/S progression.

The ability of Tax to shorten the length of G1 and to accelerate cells into S (70) embodies a constitutive (i.e. DNA damage-independent) and a DNA damage-induced component. Thus, direct Tax binding of Cdk4 and its enhancement of CycD-Cdk4 activity (55) occur constitutively and are independent of any DNA damage-triggered events. At the same time, Tax can also subvert DNA damage-induced G1 arrest enforced through p53 (71–74) (see more below). Currently, how Tax affects other phases of the cell cycle is less clear. Emerging findings suggest that this viral oncoprotein can also impair the DNA damage-induced checkpoint in G2/M transition (75, 76).


   Tax and Structurally Damaged Chromosomes
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 
Cancer is a genetic disease. It is estimated that cancer cells can contain more than 100,000 discrete mutations (77). All cancers can be broadly divided into two groups (reviewed in Ref. 78): those arising from loss of DNA repair function (and therefore have structurally damaged chromosomes) and those with chromosomal instability (and therefore have polypoidy and/or aneuploidy). Clastogenic DNA damage is frequently found in HTLV-I-transformed cells (79) and cells transfected to express Tax (80) (Fig. 2A). Clastogenic changes (point mutations, deletions, substitutions, translocations) arise and persist when defects in DNA repair mechanisms co-exist in a cell with a loss in checkpoint functions that would normally eliminate damaged DNA.



View larger version (56K):
[in this window]
[in a new window]
  		FIG. 2.
Tax causes chromosomal mis-segregation and chromosomal breakage and fusion events. A–C, examples of monkey fibroblast cells that were transfected with Tax and stained 48 h later with propidium iodide and anti-kinetochore antisera. Arrows point to small aberrant sacules of DNA, commonly termed micronuclei. Intensely stained dots within micronuclei indicate the presence of kinetechores, which reflect inappropriate segregation of centromere-containing chromosomes. D, an example of a chromosome from Tax-expressing cells that exhibit multiple breakage and fusion events. Bright interstitial dots in the chromosome represent in situ hybridization with a telomere-specific probe. The six telomere spots indicate that this chimeric chromosome has undergone a minimum of two breakage and fusion events.

 
All cells acquire DNA damage at a low frequency as they transit the cell cycle. Several mechanisms, including base excision repair (BER), nucleotide excision repair (NER), recombination, and direct repair of nicks by DNA ligation act to correct genetic mistakes. In 1990, the first clue that HTLV-I subverts cellular DNA repair came from the finding that Tax repressed the expression of DNA polymerase {beta}, an enzyme involved in BER (81). Subsequently, reduced BER activity was confirmed in HTLV-I, HTLV-II, and bovine leukemia virus-transformed cells (82). Next, Tax was found to suppress the NER normally observed following UV irradiation of cells (83). NER requires DNA polymerases {delta} and {epsilon} and uses proliferating cell nuclear antigen (PCNA) as a cofactor. Excessive PCNA can prompt DNA polymerase {delta} to synthesize inappropriately new DNA past template lesions, resulting in nucleotide misincorporation (84). Tax is believed to inhibit NER through its transcriptional up-regulation of PCNA (85); this inhibition of NER also depends, in part, on Tax's inactivation of p53 function (71–74).

There is no evidence that Tax interferes with DNA ligation (86) or DNA recombination. However, recent data suggest that Tax represses the expression of human telomerase (hTert) (87). Repression of telomerase is significant because the telomeric repeats of chromosomes normally prevent aberrant end-to-end fusions (Fig. 2B) and protect the ends from degradation by exonucleases. Furthermore, de novo double-stranded breaks in chromosomes can also be stabilized by the transient addition of telomeric repeats (88–90). Indeed, we have documented that Tax prevents such addition of telomeric repeats to new double-stranded breaks (91) and in this way potentially interferes with a protective mechanism used to prevent inappropriate breakages-fusions (Fig. 2B). The combined effects of Tax on BER, NER, DNA end stability, telomerase, and cell cycle progression create a setting in which repair of mistakes is compromised. These combined dysregulations might explain the observed 2.8-fold increase in genomic mutation frequency (92) in HTLV-I-infected cells.


   Tax and Aneuploidy
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 
The majority of cancers are aneuploid (93). In transformed cells, numerical chromosomal changes that include losses or gains of entire chromosomes (aneuploidy) generally co-exist with structural chromosomal damage.2 Although controversial, increasingly aneuploidy is thought to be a cause, rather than a consequence, of transformation (95).

During normal mitosis, human diploid cells maintain euploidy by precisely partitioning 23 pairs of chromosomes from a mother cell to two daughter cells. ATL cells, by contrast, are famously aneuploid (reviewed in Ref. 79). Their nuclei are highly lobulated or convoluted, earning them the name of "flower" cells. This suggests that a cellular mechanism that guards against chromosomal missegregation in mitosis is also subverted by HTLV-I. The mitotic spindle assembly checkpoint (MSC) (96) is a key guardian of euploidy. Interestingly, when several ATL cell lines were tested ex vivo, all were found to be deficient in MSC function (97). A potential explanation for this loss arises from two findings: (a) Tax binds human Mad1 (98, 99) and (b) Mad1 is an integral constituent of the MSC (96). That impairment of Mad1 function by Tax may contribute to ATL pathogenesis finds intriguing support in the clinical courses of non-HTLV-I acute myeloid leukemia (AML). In two large AML series (1213 and 1612 patients, respectively), loss of a single chromosome 7 (note that the gene for human Mad1 maps to chromosome 7 (100)) prognosticated an extremely poor outcome (101, 102). In these two studies, whereas all AML patients had 5-year overall survival rates of 24–44%, counterpart AML patients with monosomy 7 had survival rates of 0–10%, respectively (101, 102). Other explanations not excluded, a tantalizing parallel between the two leukemias is that one (ATL) impairs Mad1 function through viral oncoprotein subversion whereas the other (AML) does so through physical loss of chromosome 7 (i.e. monosomy 7).

Is loss of MSC the sole reason for aneuploidy in ATL cells? The answer appears to be "no." Conceptually, one recognizes that loss of checkpoint can explain the tolerance of mistakes by cells, but checkpoint loss cannot create de novo mistakes. Recent studies suggest that Tax might directly trigger chromosomal separation errors in two ways. First, Tax can promote the unscheduled degradation of securin and cyclin B1 most likely through the premature activation of the CDC20-associated anaphase promoting complex (103), thereby leading to faulty mitosis. Second, like the human papilloma virus E7 oncoprotein (38), Tax can also induce aberrant centrosomal multiplication in G1.3 Generating supernumerary centrosomes results in multipolar mitosis, which is another mechanism for creating aneuploidy (104).

Finally, there is a school of thought that suggests polyploidy as the precursor of aneuploidy (104). Relevant to this notion, we note that Tax expression does facilely create multinucleated (i.e. polyploid) cells (76, 98). Add to this the fact that Tax can inactivate p53 and Rb (65, 71–74), two factors essential to a G1 tetraploid/polypoid checkpoint (105), and one then can further envision how this might be yet another route traveled by HTLV-I/Tax/ATL cells toward aneuploidy (Fig. 3).



View larger version (19K):
[in this window]
[in a new window]
  		FIG. 3.
A flow diagram of the various routes that Tax could use to generate aneuploidy in cells. It is emphasized that two discrete events, a damage-initiating stimulus plus the loss of a checkpoint, are required for genetic mistakes to become fixated into the genome.

 

   Proliferation versus Apoptosis
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
Concluding Comments
 REFERENCES
 
A long standing cancer paradox is that overexpression of oncogenes does not simply provide proliferative advantages to cells but frequently also triggers cells to undergo apoptosis. Findings from oncogenic transcription factors such as Myc, E1A, and E2F-1 show this duality to be the rule rather than the exception (reviewed in Ref. 106). Indeed, it is now apparent that oncogenic insults induce countervailing responses by the cell, which are reflected in cell cycle arrest and apoptosis. We reviewed, above, how Tax defeats cellular mechanisms for braking cell cycle progression. No cell cycle and/or genetic instability manifestations of Tax can confer selective growth advantage if cells fail to tolerate such phenotypic and genotypic changes and choose instead apoptotic death. Hence, disabling the cellular apoptotic response remains a requisite for transformation.

By definition, the clinical presentation of ATL implies that in a subpopulation of CD4+ T-cells, HTLV-I infection tips the balance between proliferation and apoptosis toward the former. Nevertheless, how HTLV-I Tax oncoprotein influences this choice is not fully understood. Many have examined the contribution of Tax to stress-induced apoptosis. Overall findings have been controversial and divergent. Some found that Tax protects cells from stress-induced cell cycle arrest or apoptosis (107–109), whereas others observed that Tax sensitizes cells to stress-induced apoptosis (110–113). Likely, the decision between proliferation and death is influenced by the cellular environment, cell type genetic background, and multiple co-existing signaling events. Depending on context, which set of genes that Tax transcriptionally activates (31) and/or which cluster of gene products that Tax binds (94) will mean either the normal cellular response against oncogenic stress will either prevail (i.e. apoptosis) or be subverted (i.e. proliferation) by HTLV-I. A clear understanding of factors in addition to Tax that guide this choice for HTLV-I-infected T-cells will be a major topic for future research.


   Concluding Comments
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
REFERENCES
 
Over 20 million individuals globally are infected with HTLV-I. It is estimated that 2–5% of these carriers will develop ATL over their lifetime. The identification and isolation of HTLV-I 25 years ago have spurred intensive mechanistic investigations into ATL transformation. Using Tax as a model system, we have learned that viral means for transformation parallel similar mechanistic changes seen in spontaneously occurring cancers. A simplified sequence of events appears to be genetic damage initiated by oncogenic stimuli, followed by subversion of cellular checks allowing tolerance and fixation of changes into the genome, and finally selection over time for the correct mix of gene alterations that confer selective growth advantage. Clearly the process is complex and multifaceted. Fleshing out all the biological and molecular details to accompany this simplified framework will easily keep HTLV researchers busy for another 25 years.


   FOOTNOTES
 
* This minireview will be reprinted in the 2004 Minireview Compendium, which will be available in January, 2005. Back

§ To whom correspondence should be addressed: Bldg. 4, Rm. 306, NIH, 9000 Rockville Pike, Bethesda, MD 20892. Tel.: 301-496-6680; Fax: 301-480-3686; E-mail: kj7e{at}nih.gov.

1 The abbreviations used are: HTLV-I, human T-cell leukemia virus type I; ATL, adult T-cell leukemia; LTR, long terminal repeat; IL, interleukin; CDK, cyclin-dependent kinase; BER, base excision repair; NER, nucleotide excision repair; PCNA, proliferating cell nuclear antigen; MSC, mitotic spindle assembly checkpoint; AML, acute myeloid leukemia. Back

2 F. Mitelman, B. Johansson, and F. Mertens, personal communication. Back

3 K. Haller and K. T. Jeang, unpublished data. Back


   ACKNOWLEDGMENTS
 
We thank Fatah Kashanchi for critical reading of the manuscript and Lan Lin for preparation of figures and text.



   REFERENCES
TOP
 INTRODUCTION
 The Molecular Biology of...
 Tax and Cell Cycle...
 Tax and Structurally Damaged...
 Tax and Aneuploidy
 Proliferation versus Apoptosis
 Concluding Comments
 REFERENCES
 

  1. Poiesz, B. J., Ruscetti, F. W., Gadzar, A. F., Bunn, P. A., Minna, J. D., and Gallo, R. C. (1980) Proc. Natl. Acad. Sci. U. S. A. 77, 7415–7419[Abstract/Free Full Text]
  2. Hinuma, Y., Nagata, K., Misoka, M., Nakai, T., Matsumoto, T., Kiroshita, K., Shirakwa, S., and Miyoshi, I. (1981) Proc. Natl. Acad. Sci. U. S. A. 78, 6476–6480[Abstract/Free Full Text]
  3. Matsuoka, M. (2003) Oncogene 22, 5131–5140[CrossRef][Medline] [Order article via Infotrieve]
  4. Okamoto, T., Ohno, Y., Tsugane, S., Watanabe, S., Shimoyama, M., Tajima, K., Miwa, M., and Shimotohno, K. (1989) Jpn. J. Cancer Res. 80, 191–195[CrossRef][Medline] [Order article via Infotrieve]
  5. Grassmann, R., Dengler, C., Muller-Fleckenstein, I., McGuire, K., Dokhelar, M. C., Sodroski, J. G., and Haseltine, W. A. (1989) Proc. Natl. Acad. Sci. U. S. A. 86, 3351–3355[Abstract/Free Full Text]
  6. Ross, T. M., Pettiford, S. M., and Green, P. L. (1996) J. Virol. 70, 5194–5202[Abstract/Free Full Text]
  7. Tanaka, A., Takahashi, G., Yamaoka, S., Nosaka, T., Maki, M., and Hatanaka, M. (1990) Proc. Natl. Acad. Sci. U. S. A. 87, 1071–1075[Abstract/Free Full Text]
  8. Nerenberg, M., Hinrichs, S. H., Reynolds, R. K., Khoury, G., and Jay, G. (1987) Science 237, 1324–1329[Abstract/Free Full Text]
  9. Grossman, W. J., Kimata, J. T., Wong, F. H., Zutter, M., Ley, T. J., and Ratner, L. (1995) Proc. Natl. Acad. Sci. U. S. A. 14, 1057–1061
  10. Kinzler, K. W., and Vogelstein, B. (1996) Cell 87, 159–170[CrossRef][Medline] [Order article via Infotrieve]
  11. Richardson, J. H., Edwards, A. J., Cruickshank, J. K., Rudge, P., and Dalgleish, A. G. (1990) J. Virol. 64, 5682–5687[Abstract/Free Full Text]
  12. Nagai, M., Brennan, M. B., Sakai, J. A., Mora, C. A., and Jacobson, S. (2001) Blood 98, 1858–1861[Medline] [Order article via Infotrieve]
  13. Okochi, K., and Sato, H. (1984) Princess Takamatsu Symp. 15, 129–135[Medline] [Order article via Infotrieve]
  14. Igakura, T., Stinchcombe, J. C., Goon, P. K., Taylor, G. P., Weber, J. N., Griffiths, G M., Tanaka, Y., Osame, M., and Bangham, C. R. (2003) Science 299, 1713–1716[Abstract/Free Full Text]
  15. Manel, N., Kim, F. J., Kinet, S., Taylor, N., Sitbon, M., and Battini, J. L. (2003) Cell 115, 449–459[CrossRef][Medline] [Order article via Infotrieve]
  16. Semmes, O. J., and Jeang, K. T. (1996) J. Virol. 70, 6347–6357[Abstract]
  17. Burton, M., Upadhyaya, C. D., Maier, B., Hope, T. J., and Semmes, O. J. (2000) J. Virol. 74, 2351–2364[Abstract/Free Full Text]
  18. Twizere, J. C., Kruys, V., Lefebvre, L., Vanderplasschen, A., Collete, D., Debacq, C., Lai, W. S., Jauniaux, J. C., Bernstein, L. R., Semmes, O. J., Burny, A., Blackshear, P. J., Kettmann, R., and Willems, L. (2003) J. Natl. Cancer Inst. 95, 1846–1859[Abstract/Free Full Text]
  19. Carman, J. A., and Nadler, S. G. (2004) Biochem. Biophys. Res. Commun. 315, 445–449[Medline] [Order article via Infotrieve]
  20. Seiki, M., Inoue, J., Takeda, T., and Yoshida, M. (1986) EMBO J. 5, 561–565[Medline] [Order article via Infotrieve]
  21. Brady, J., Jeang, K. T., Duvall, J., and Khoury, G. (1987) J. Virol. 61, 2175–2181[Abstract/Free Full Text]
  22. Jeang, K. T., Boros, I., Brady, J., Radonovich, M., and Khoury, G. (1988) J. Virol. 62, 4499–4509[Abstract/Free Full Text]
  23. Inoue, J., Seiki, M., Taniguchi, T., Tsuru, S., and Yoshida, M. (1986) EMBO J. 5, 2883–2888[Medline] [Order article via Infotrieve]
  24. Cross, S. L., Feinberg, M. B., Wolf, J. B., Holbrook, N. J., Wong-Staal, F., and Leonard, W. J. (1987) Cell 49, 47–56[CrossRef][Medline] [Order article via Infotrieve]
  25. Siekevitz, M., Feinberg, M. B., Holbrook, N., Wong-Staal, F., and Greene, W. C. (1987) Proc. Natl. Acad. Sci. U. S. A. 85, 5389–5393
  26. Fujii, M., Sassone-Corsi, P., and Verma, I. M. (1988) Proc. Natl. Acad. Sci. U. S. A. 85, 8526–8530[Abstract/Free Full Text]
  27. Nagata, K., Ohtani, K., Nakamura, M., and Sagamura, K. (1989) J. Virol. 63, 3220–3226[Abstract/Free Full Text]
  28. Miyatake, S., Seiki, M., Yoshida, M., and Arai, K. (1988) Mol. Cell. Biol. 8, 5581–5587[Abstract/Free Full Text]
  29. Azimi, N., Brown, K., Bamford, R. N., Tagaya, Y., Siebenlist, U., and Waldmann, T. A. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 2452–2457[Abstract/Free Full Text]
  30. Chung, H. K., Young, H. A., Goon, P. K., Heidecker, G., Princler, G. L., Shimozato, O., Taylor, G. P., Bangham, C. R., and Derse, D. (2003) Blood 102, 4130–4136[Abstract/Free Full Text]
  31. Ng, P. W., Iha, H., Iwanaga, Y., Bittner, M., Chen, Y., Jiang, Y., Gooden, G., Trent, J. M., Meltzer, P., Jeang, K. T., and Zeichner, S. L. (2001) Oncogene 20, 4484–4496[CrossRef][Medline] [Order article via Infotrieve]
  32. Mesnard, J. M., and Devaux, C. (1999) Virology 257, 277–284[CrossRef][Medline] [Order article via Infotrieve]
  33. Sun, S. C., and Ballard, D. W. (1999) Oncogene 18, 6948–6958[CrossRef][Medline] [Order article via Infotrieve]
  34. Jeang, K. T., Chiu, R., Santos, E., and Kim, S. J. (1991) Virology 181, 218–227[CrossRef][Medline] [Order article via Infotrieve]
  35. Fujii, M., Tsuchiya, J., Chuhjo, T., Akizawa, T., and Seiki, M. (1992) Genes Dev. 6, 2066–2076[Abstract/Free Full Text]
  36. Jeang, K. T. (2001) Cytokine Growth Factor Rev. 12, 207–217[CrossRef][Medline] [Order article via Infotrieve]
  37. Helt, A. M., and Galloway, D. A. (2003) Carcinogenesis 24, 159–169[Abstract/Free Full Text]
  38. Duensing, S., and Munger, K. (2003) Crit. Rev. Eukaryotic Gene Expression 13, 9–23[CrossRef][Medline] [Order article via Infotrieve]
  39. Lavia, P., Mileo, A. M., Giordano, A., and Paggi, M. G. (2003) Oncogene 22, 6508–6516[CrossRef][Medline] [Order article via Infotrieve]
  40. Hunter, T., and Pines, J. (1994) Cell 79, 573–582[CrossRef][Medline] [Order article via Infotrieve]
  41. Sherr, C. J., and Roberts, J. M. (1999) Genes Dev. 13, 1501–1512[Free Full Text]
  42. Matsushime, H., Quelle, D. E., Shurtleff, S. A., Shibuya, M., Sherr, C. J., and Kato, J. Y. (1994) Mol. Cell. Biol. 14, 2066–2076[Abstract/Free Full Text]
  43. Resnitzky, D., Gossen, M., Bujard, H., and Reed, S. I. (1994) Mol. Cell. Biol. 14, 1669–1679[Abstract/Free Full Text]
  44. Sherr, C. J. (1994) Cell 79, 551–555[CrossRef][Medline] [Order article via Infotrieve]
  45. Grana, X., and Reddy E. P. (1995) Oncogene 11, 211–219[Medline] [Order article via Infotrieve]
  46. Bell, L. A., and Ryan, K. M. (2004) Cell Death Differ. 11, 137–142[CrossRef][Medline] [Order article via Infotrieve]
  47. Dowdy, S. F., Hinds, P. W., Louie, K., Reed, S. I., Arnold, A., and Weinberg, R. A. (1993) Cell 73, 499–511[CrossRef][Medline] [Order article via Infotrieve]
  48. Ewen, M. E., Sluss, H. K., Sherr, C. J., Matsushime, H., Kato, J., and D. M. (1993) Cell 73, 487–497[CrossRef][Medline] [Order article via Infotrieve]
  49. Suzuki, T., Kitao, S., Matsushime, H., and Yoshida, M. (1996) EMBO J. 15, 1607–1614[Medline] [Order article via Infotrieve]
  50. Low, K. G., Dorner, L. F., Fernando, D. B., Grossman, J., Jeang, K. T., and Comb, M. J. (1997) J. Virol. 71, 1956–1962[Abstract]
  51. Iwanaga, R., Ohtani, K., Hayashi, T., and Nakamura, M. (2001) Oncogene 20, 2055–2067[CrossRef][Medline] [Order article via Infotrieve]
  52. Huang, Y., Ohtani, K., Iwanaga, R., Matsumura, Y., and Nakamura, M. (2001) Oncogene 20, 1094–1102[CrossRef][Medline] [Order article via Infotrieve]
  53. Akagi, T., Ono, H., and Shimotohno, K. (1996) Oncogene 12, 1645–1652[Medline] [Order article via Infotrieve]
  54. de La Fuente, C., Santiago, F., Chong, S. Y., Deng, L., Mayhood, T., Fu, P., Stein, D., Denny, T., Coffman, F., Azimi, N., Mahieux, R., and Kashanchi, F. (2000) J. Virol. 74, 7270–7283[Abstract/Free Full Text]
  55. Haller, K., Wu, Y., Derow, E., Schmitt, I., Jeang, K. T., and Grassmann, R. (2002) Mol. Cell. Biol. 22, 3327–3338[Abstract/Free Full Text]
  56. Wilson, K. C., Center, D. M., Cruikshank, W. W., and Zhang, Y. (2003) Virology 306, 60–67[CrossRef][Medline] [Order article via Infotrieve]
  57. Suzuki, T., Narita, T., Uchida-Toita, M., and Yoshida, M. (1999) Virology 259, 384–391[CrossRef][Medline] [Order article via Infotrieve]
  58. Kibler, K. V., and Jeang, K. T. (2001) J. Virol. 75, 2161–2173[Abstract/Free Full Text]
  59. Cereseto, A., Washington Parks, R., Rivadeneira, E., and Franchini, G. (1999) Oncogene 18, 2441–2450[CrossRef][Medline] [Order article via Infotrieve]
  60. Santiago, F., Clark, E., Chong, S., Molina, C., Mozafari, F., Mahieux, R., Fujii, M., Azimi, N., and Kashanchi, F. (1999) J. Virol. 73, 9917–9927[Abstract/Free Full Text]
  61. Kawata, S., Ariumi, Y., and Shimotohno, K. (2003) J. Virol. 77, 7291–7299[Abstract/Free Full Text]
  62. Chowdhury, I. H., Farhadi, A., Wang, X. F., Robb, M. L., Birx, D. L., and Kim, J. H. (2003) Int. J. Cancer 107, 603–611[CrossRef][Medline] [Order article via Infotrieve]
  63. Schavinsky-Khrapunsky, Y., Huleihel, M., Aboud, M., and Torgeman, A. (2003) Oncogene 22, 5315–5324[Medline] [Order article via Infotrieve]
  64. Lemasson, I., Thebault, S., Sardet, C., Devaux, C., and Mesnard, J. M. (1998) J. Biol. Chem. 273, 23598–23604[Abstract/Free Full Text]
  65. Neuveut, C., Low, K. G., Maldarelli, F., Schmitt, I., Majone, F., Grassmann, R., and Jeang, K. T. (1998) Mol. Cell. Biol. 18, 3620–3632[Abstract/Free Full Text]
  66. Ohtani, K., Iwanaga, R., Arai, M., Huang, Y., Matsumura, Y., and Nakamura, M. (2000) J. Biol. Chem. 275, 11154–11163[Abstract/Free Full Text]
  67. LaBaer, J., Garrett, M. D., Stevenson, L. F., Slingerland, J. M., Sandhu, C., Chou, H. S., Fattaey, A., and Harlow, E. (1997) Genes Dev. 11, 847–862[Abstract/Free Full Text]
  68. Zhang, H., Hannon, G. J., and Beach, D. (1994) Genes Dev. 8, 1750–1758[Abstract/Free Full Text]
  69. Kehn, K., Deng, L., de la Fuente, C., Strouss, K., Wu, K., Maddukkuri, A., Baylor, S., Rufner, R., Pumfery, A., Bottazzi, M. E., and Kashanchi, F. (2004) Retrovirology 1, 6[CrossRef][Medline] [Order article via Infotrieve]
  70. Lemoine, F. J., and Marriott, S. J. (2001) J. Biol. Chem. 276, 31851–31857[Abstract/Free Full Text]
  71. Pise-Masison, C. A., Choi, K. S., Radonovich, M., Dittmer, J., Kim, S. J., and Brady, J. N. (1998) J. Virol. 72, 1165–1170[Abstract/Free Full Text]
  72. Akagi, T., Ono, H., Tsuchida, N., and Shimotohno, K. (1997) FEBS Lett. 406, 263–266[CrossRef][Medline] [Order article via Infotrieve]
  73. Takemoto, S., Trovato, R., Cereseto, A., Nicot, C., Kislyakova, T., Casareto, L., Waldmann, T., Torelli, G., and Franchini, G. (2000) Blood 95, 3939–3944[Abstract/Free Full Text]
  74. Van, P. L., Yim, K. W., Jin, D. Y., Dapolito, G., Kurimasa, A., and Jeang, K. T. (2001) J. Virol. 75, 396–407[Abstract/Free Full Text]
  75. Haoudi, A., Daniels, R. C., Wong, E., Kupfer, G., and Semmes, O. J. (2003) J. Biol. Chem. 278, 37736–37744[Abstract/Free Full Text]
  76. Liang, M. H., Geisbert, T., Yao, Y., Hinrichs, S. H., and Giam, C. Z. (2002) J. Virol. 76, 4022–4033[Abstract/Free Full Text]
  77. Perucho, M. (1996) J. Biol. Chem. 377, 677–684
  78. Loeb, K. R., and Loeb L. A. (2000) Carcinogenesis 21, 379–385[Abstract/Free Full Text]
  79. Marriott, S. J., Lemoine, F. J., and Jeang, K. T. (2002) J. Biomed. Sci. 9, 292–298[Medline] [Order article via Infotrieve]
  80. Majone, F., Semmes, O. J., and Jeang, K. T. (1993) Virology 193, 456–459[CrossRef][Medline] [Order article via Infotrieve]
  81. Jeang, K. T., Widen, S. G., Semmes, O. J., and Wilson, S. H. (1990) Science 247, 1082–1084[Abstract/Free Full Text]
  82. Philpott, S. M., and Buehring, G. C. (1999) J. Natl. Cancer Inst. 91, 933–942[Abstract/Free Full Text]
  83. Kao, S. Y., and Marriott, S. J. (1999) J. Virol. 73, 4299–4304[Abstract/Free Full Text]
  84. Mozzherin, D. J., Shibutani, S., Tan, C. K., Downey, K. M., and Fisher, P. A. (1997) Proc. Natl. Acad. Sci. U. S. A. 94, 6126–6131[Abstract/Free Full Text]
  85. Lemoine, F. J., Kao, S-Y., and Marriott, S. J. (2000) AIDS Res. Hum. Retroviruses 16, 1623–1627[CrossRef][Medline] [Order article via Infotrieve]
  86. Kao, S-Y., and Marriott, S. J. (2000) J. Biol. Chem. 275, 35926–35931[Abstract/Free Full Text]
  87. Gabet, A. S., Mortreux, F., Charneau, P., Riou, P., Duc-Dodon, M., Wu, Y., Jeang, K. T., and Wattel, E. (2003) Oncogene 22, 3734–3741[CrossRef][Medline] [Order article via Infotrieve]
  88. Morin, G. B. (1991) Nature 353, 454–456[CrossRef][Medline] [Order article via Infotrieve]
  89. Wilkie, A. O., Lamb, J., Harris, P. C., Finney, R. D., and Higgs, D. R. (1990) Nature 346, 868–871[CrossRef][Medline] [Order article via Infotrieve]
  90. Flint, J., Craddock, C. F., Villegas, A., Bentley, D. P., Williams, H. J., Galanello, R., Cao, A., Wood, W. G., Ayyub, H., and Higgs, D. R. (1994) Am. J. Hum. Genet. 55, 505–512[Medline] [Order article via Infotrieve]
  91. Majone, F., and Jeang, K. T. (2000) J. Biol. Chem. 275, 32906–32910[Abstract/Free Full Text]
  92. Miyake, H., Suzuki, T., Hirai, H., and Yoshida, M. (1999) Virology 253, 155–161[CrossRef][Medline] [Order article via Infotrieve]
  93. Cahill, D. P., Lengauer, C., Yu, J., Riggins, G. J., Willson, J. K., Markowitz, S. D., Kinzler, K. W., and Vogelstein, B. (1998) Nature 392, 300–303[CrossRef][Medline] [Order article via Infotrieve]
  94. Wu, K., Bottazzi, M. E., de la Fuente, C., Deng, L., Gitlin, S. D., Maddukuri, A., Dadgar, S., Li, H., Vertes, A., Pumfery, A., and Kashanchi, F. (2004) J. Biol. Chem. 279, 495–508[Abstract/Free Full Text]
  95. Rasnick, D. (2002) Cancer Genet. Cytogenet. 136, 66–72[CrossRef][Medline] [Order article via Infotrieve]
  96. Musacchio, A., and Hardwick, K. G. (2002) Nat. Rev. Mol. Cell. Biol. 3, 731–741[CrossRef][Medline] [Order article via Infotrieve]
  97. Kasai, T., Iwanaga, Y., Iha, H., and Jeang, K. T. (2002) J. Biol. Chem. 277, 5187–5193[Abstract/Free Full Text]
  98. Jin, D. Y., Spencer, F., and Jeang, K. T. (1998) Cell 93, 81–91[CrossRef][Medline] [Order article via Infotrieve]
  99. Iwanaga, Y., Kasai, T., Kibler, K., and Jeang, K. T. (2002) J. Biol. Chem. 277, 31005–31013[Abstract/Free Full Text]
  100. Jin, D. Y., Kozak, C. A., Pangilinan, F., Spencer, F., Green, E. D., and Jeang, K. T. (1999) Genomics 55, 363–364[CrossRef][Medline] [Order article via Infotrieve]
  101. Byrd, J. C., Mrozek, K., Dodge, R. K., Carroll, A. J., Edwards, C. G., Pettenati, M. J., Patil, S. R., Rao, K. W., Watson, M. S., Koduru, P. R., Moore, J. O., Stone, R. M., Mayer, R. J., Feldman, E. J., Davey, F. R., Schiffer, C. A., Larson, R. A., Bloomfield, C. D., and Cancer and Leukemia Group B (CALGB 8461) (2002) Blood 100, 4325–4336[Abstract/Free Full Text]
  102. Grimwade, D., Walker, H., Oliver, F., Wheatley, K., Harrison, C., Harrison, G., Rees, J., Hann, I., Stevens, R., Burnett, A., and Goldstone, A. (1998) Blood 92, 2322–2333[Abstract/Free Full Text]
  103. Liu, B., Liang, M. H., Kuo, Y. L., Liao, W., Boro, I., Kleinberger, T., Blancato, J., and Giam, C. Z. (2003) Mol. Cell. Biol. 23, 5269–5281[Abstract/Free Full Text]
  104. Storchova, Z., and Pellman, D. (2004) Nat. Rev. Mol. Cell. Biol. 5, 45–54[CrossRef][Medline] [Order article via Infotrieve]
  105. Margolis, R. L., Lohez, O. D., and Andreassen, P. R. (2003) J. Cell. Biochem. 88, 673–683[CrossRef][Medline] [Order article via Infotrieve]
  106. Nilsson, J. A., and Cleveland, J. L. (2003) Oncogene 22, 9007–9021[CrossRef][Medline] [Order article via Infotrieve]
  107. Torgeman, A., Ben-Aroya, Z., Grunspan, A., Zelin, E., Butovsky, E., Hallak, M., Lochelt, M., Flugel, R. M., Livneh, E., Wolfson, M., Kedar, I., and Aboud, M. (2001) Exp. Cell Res. 271, 169–179[CrossRef][Medline] [Order article via Infotrieve]
  108. Brauweiler, A., Garrus, J. E., Reed, J. C., and Nyborg, J. K. (1997) Virology 231, 135–140[CrossRef][Medline] [Order article via Infotrieve]
  109. Copeland, K. F., Haaksma, A. G., Goudsmit, J., Krammer, P. H., and Heeney, J. L. (1994) AIDS Res. Hum. Retroviruses 10, 1259–1268[Medline] [Order article via Infotrieve]
  110. Chlichlia, K., Moldenhauer, G., Daniel, P. T., Busslinger, M., Gazzolo, L., Schirmacher, V., and Khazaei, K. (1995) Oncogene 10, 269–277[Medline] [Order article via Infotrieve]
  111. Chlichlia, K., Busslinger, M., Peter, M. E., Walczak, H., Krammer, P., Schirrmacher, V., and Khazaie, K. (1997) Oncogene 14, 2265–2272[CrossRef][Medline] [Order article via Infotrieve]
  112. Kao, S. Y., Leomine, F. J., and Marriott, S. J. (2000) Oncogene 19, 2240–2248[CrossRef][Medline] [Order article via Infotrieve]
  113. Kasai, T., and Jeang, K. T. (2004) Retrovirology 1, 7[CrossRef][Medline] [Order article via Infotrieve]

Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Virol.Home page
K. A. Fryrear, S. S. Durkin, S. K. Gupta, J. B. Tiedebohl, and O. J. Semmes
Dimerization and a Novel Tax Speckled Structure Localization Signal Are Required for Tax Nuclear Localization
J. Virol., June 1, 2009; 83(11): 5339 - 5352.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
J.-M. Peloponese Jr., J. Yasunaga, T. Kinjo, K. Watashi, and K.-T. Jeang
Peptidylproline cis-trans-Isomerase Pin1 Interacts with Human T-Cell Leukemia Virus Type 1 Tax and Modulates Its Activation of NF-{kappa}B
J. Virol., April 1, 2009; 83(7): 3238 - 3248.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
K.-J. Jung, A. Dasgupta, K. Huang, S.-J. Jeong, C. Pise-Masison, K. V. Gurova, and J. N. Brady
Small-Molecule Inhibitor Which Reactivates p53 in Human T-Cell Leukemia Virus Type 1-Transformed Cells
J. Virol., September 1, 2008; 82(17): 8537 - 8547.
[Abstract] [Full Text] [PDF]

Home page
 Antimicrob. Agents Chemother.Home page
E. Balestrieri, C. Matteucci, A. Ascolani, A. Piperno, R. Romeo, G. Romeo, U. Chiacchio, A. Mastino, and B. Macchi
Effect of Phosphonated Carbocyclic 2'-Oxa-3'-Aza-Nucleoside on Human T-Cell Leukemia Virus Type 1 Infection In Vitro
Antimicrob. Agents Chemother., January 1, 2008; 52(1): 54 - 64.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
N. Shembade, N. S. Harhaj, M. Yamamoto, S. Akira, and E. W. Harhaj
The Human T-Cell Leukemia Virus Type 1 Tax Oncoprotein Requires the Ubiquitin-Conjugating Enzyme Ubc13 for NF-{kappa}B Activation
J. Virol., December 15, 2007; 81(24): 13735 - 13742.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. K. Gupta, X. Guo, S. S. Durkin, K. F. Fryrear, M. D. Ward, and O. J. Semmes
Human T-cell Leukemia Virus Type 1 Tax Oncoprotein Prevents DNA Damage-induced Chromatin Egress of Hyperphosphorylated Chk2
J. Biol. Chem., October 5, 2007; 282(40): 29431 - 29440.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
T. Hishiki, T. Ohshima, T. Ego, and K. Shimotohno
BCL3 Acts as a Negative Regulator of Transcription from the Human T-cell Leukemia Virus Type 1 Long Terminal Repeat through Interactions with TORC3
J. Biol. Chem., September 28, 2007; 282(39): 28335 - 28343.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
S. V. Sheleg, J.-M. Peloponese, Y.-H. Chi, Y. Li, M. Eckhaus, and K.-T. Jeang
Evidence for Cooperative Transforming Activity of the Human Pituitary Tumor Transforming Gene and Human T-Cell Leukemia Virus Type 1 Tax
J. Virol., August 1, 2007; 81(15): 7894 - 7901.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
M. Merimi, P. Klener, M. Szynal, Y. Cleuter, P. Kerkhofs, A. Burny, P. Martiat, and A. Van den Broeke
Suppression of Viral Gene Expression in Bovine Leukemia Virus-Associated B-Cell Malignancy: Interplay of Epigenetic Modifications Leading to Chromatin with a Repressive Histone Code
J. Virol., June 1, 2007; 81(11): 5929 - 5939.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
T. Tsuji, N. Sheehy, V. W. Gautier, H. Hayakawa, H. Sawa, and W. W. Hall
The Nuclear Import of the Human T Lymphotropic Virus Type I (HTLV-1) Tax Protein Is Carrier- and Energy-independent
J. Biol. Chem., May 4, 2007; 282(18): 13875 - 13883.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
J.-C. Twizere, J.-Y. Springael, M. Boxus, A. Burny, F. Dequiedt, J.-F. Dewulf, J. Duchateau, D. Portetelle, P. Urbain, C. V. Lint, et al.
Human T-cell leukemia virus type-1 Tax oncoprotein regulates G-protein signaling
Blood, February 1, 2007; 109(3): 1051 - 1060.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
C. Debacq, N. Gillet, B. Asquith, M. T. Sanchez-Alcaraz, A. Florins, M. Boxus, I. Schwartz-Cornil, M. Bonneau, G. Jean, P. Kerkhofs, et al.
Peripheral Blood B-Cell Death Compensates for Excessive Proliferation in Lymphoid Tissues and Maintains Homeostasis in Bovine Leukemia Virus-Infected Sheep
J. Virol., October 1, 2006; 80(19): 9710 - 9719.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
S. Calattini, S. A. Chevalier, R. Duprez, P. Afonso, A. Froment, A. Gessain, and R. Mahieux
Human T-Cell Lymphotropic Virus Type 3: Complete Nucleotide Sequence and Characterization of the Human Tax3 Protein
J. Virol., October 1, 2006; 80(19): 9876 - 9888.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
Y.-T. Siu, K.-T. Chin, K.-L. Siu, E. Yee Wai Choy, K.-T. Jeang, and D.-Y. Jin
TORC1 and TORC2 Coactivators Are Required for Tax Activation of the Human T-Cell Leukemia Virus Type 1 Long Terminal Repeats
J. Virol., July 15, 2006; 80(14): 7052 - 7059.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
A. Krueger, S. C. Fas, M. Giaisi, M. Bleumink, A. Merling, C. Stumpf, S. Baumann, D. Holtkotte, V. Bosch, P. H. Krammer, et al.
HTLV-1 Tax protects against CD95-mediated apoptosis by induction of the cellular FLICE-inhibitory protein (c-FLIP)
Blood, May 15, 2006; 107(10): 3933 - 3939.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
M. Zhou, H. Lu, H. Park, J. Wilson-Chiru, R. Linton, and J. N. Brady
Tax Interacts with P-TEFb in a Novel Manner To Stimulate Human T-Lymphotropic Virus Type 1 Transcription.
J. Virol., May 1, 2006; 80(10): 4781 - 4791.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
Y. Tabakin-Fix, I. Azran, Y. Schavinky-Khrapunsky, O. Levy, and M. Aboud
Functional inactivation of p53 by human T-cell leukemia virus type 1 Tax protein: mechanisms and clinical implications
Carcinogenesis, April 1, 2006; 27(4): 673 - 681.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J.-M. Peloponese Jr. and K.-T. Jeang
Role for Akt/Protein Kinase B and Activator Protein-1 in Cellular Proliferation Induced by the Human T-cell Leukemia Virus Type 1 Tax Oncoprotein
J. Biol. Chem., March 31, 2006; 281(13): 8927 - 8938.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
K. Murata, T. Hayashibara, K. Sugahara, A. Uemura, T. Yamaguchi, H. Harasawa, H. Hasegawa, K. Tsuruda, T. Okazaki, T. Koji, et al.
A Novel Alternative Splicing Isoform of Human T-Cell Leukemia Virus Type 1 bZIP Factor (HBZ-SI) Targets Distinct Subnuclear Localization
J. Virol., March 1, 2006; 80(5): 2495 - 2505.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
Y. Satou, J.-i. Yasunaga, M. Yoshida, and M. Matsuoka
HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells
PNAS, January 17, 2006; 103(3): 720 - 725.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
J.-M. Peloponese Jr., K. Haller, A. Miyazato, and K.-T. Jeang
Abnormal centrosome amplification in cells through the targeting of Ran-binding protein-1 by the human T cell leukemia virus type-1 Tax oncoprotein
PNAS, December 27, 2005; 102(52): 18974 - 18979.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. Nejmeddine, A. L. Barnard, Y. Tanaka, G. P. Taylor, and C. R. M. Bangham
Human T-lymphotropic Virus, Type 1, Tax Protein Triggers Microtubule Reorientation in the Virological Synapse
J. Biol. Chem., August 19, 2005; 280(33): 29653 - 29660.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J.-C. Twizere, L. Lefebvre, D. Collete, C. Debacq, P. Urbain, H. Heremans, J.-C. Jauniaux, A. Burny, L. Willems, and R. Kettmann
The Homeobox Protein MSX2 Interacts with Tax Oncoproteins and Represses Their Transactivation Activity
J. Biol. Chem., August 19, 2005; 280(33): 29804 - 29811.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
A. Achachi, A. Florins, N. Gillet, C. Debacq, P. Urbain, G. M. Foutsop, F. Vandermeers, A. Jasik, M. Reichert, P. Kerkhofs, et al.
Valproate activates bovine leukemia virus gene expression, triggers apoptosis, and induces leukemia/lymphoma regression in vivo
PNAS, July 19, 2005; 102(29): 10309 - 10314.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
C. Bolognesi, F. Martini, M. Tognon, R. Filiberti, M. Neri, E. Perrone, E. Landini, P. A. Canessa, G. P. Ivaldi, P. Betta, et al.
A Molecular Epidemiology Case Control Study on Pleural Malignant Mesothelioma
Cancer Epidemiol. Biomarkers Prev., July 1, 2005; 14(7): 1741 - 1746.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
M. Matsuoka and K.-T. Jeang
Human T-Cell Leukemia Virus Type I at Age 25: A Progress Report
Cancer Res., June 1, 2005; 65(11): 4467 - 4470.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
P. Hivin, M. Frederic, C. Arpin-Andre, J. Basbous, B. Gay, S. Thebault, and J.-M. Mesnard
Nuclear localization of HTLV-I bZIP factor (HBZ) is mediated by three distinct motifs
J. Cell Sci., April 1, 2005; 118(7): 1355 - 1362.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
B. Liu, S. Hong, Z. Tang, H. Yu, and C.-Z. Giam
HTLV-I Tax directly binds the Cdc20-associated anaphase-promoting complex and activates it ahead of schedule
PNAS, January 4, 2005; 102(1): 63 - 68.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
279/31/31991    most recent
R400009200v1
Right arrow Submit a Letter to Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jeang, K.-T.
Right arrow Articles by Aboud, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jeang, K.-T.
Right arrow Articles by Aboud, M.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2004 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement