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HTLV-1 bZIP Factor Induces T-Cell Lymphoma and Systemic Inflammation In Vivo
It is shown that transgenic expression of HBZ in CD4+ T cells induced T-cell lymphomas and systemic inflammation in mice, resembling diseases observed in HTLV-1 infected individuals. Expand
Comparative biology of human T-cell lymphotropic virus type 1 (HTLV-1) and HTLV-2
It has become clear that comparative studies designed to elucidate the mechanisms by which HTLV-1 andHTLV-2 determine distinct outcomes are likely to provide fundamental insights into the initiation of multistep leukemogenesis. Expand
BET proteins promote efficient murine leukemia virus integration at transcription start sites
- Amit Sharma, Ross C. Larue, +12 authors M. Kvaratskhelia
- Biology, Medicine
- Proceedings of the National Academy of Sciences
- 1 July 2013
It is shown that purified recombinant Brd4(1-720) binds with high affinity to MLV integrase and stimulates correct concerted integration in vitro and elucidate the importance of BET proteins for MLV integration efficiency and targeting and provide a route to developing safer MLV-based vectors for human gene therapy. Expand
Human T-cell leukemia virus type-1 antisense-encoded gene, Hbz, promotes T-lymphocyte proliferation.
The data indicate that Hbz expression enhances the proliferative capacity of HTLV-1-infected T cells, playing a critical role in cell survival and ultimately HTLV -1 tumorigenesis in the infected host. Expand
The HBZ gene, a key player in HTLV-1 pathogenesis
In this review, recent findings about HBZ are summarized and its roles and functions not only in the virus life cycle, but also in HTLV-1 disease pathogenesis are discussed. Expand
Enhancement of infectivity and persistence in vivo by HBZ, a natural antisense coded protein of HTLV-1.
It is indicated that HBZ was not required for in vitro cellular immortalization, but enhanced infectivity and persistence in inoculated rabbits, demonstrating that retroviruses use negative-strand-encoded proteins in the establishment of chronic viral infections. Expand
Inactivation of IkappaBbeta by the tax protein of human T-cell leukemia virus type 1: a potential mechanism for constitutive induction of NF-kappaB.
- T. McKinsey, J. Brockman, D. Scherer, S. Al-Murrani, P. Green, D. Ballard
- Biology, Medicine
- Molecular and cellular biology
- 1 May 1996
Evidence is provided that in addition to acting on IkappaBalpha, HTLV-1 Tax stimulates the turnover of IkappaBbeta via a related targeting mechanism that provides a potential mechanism for the constitutive activation of NF-kappaB in Tax-expressing cells. Expand
The human T-cell leukemia virus Rex protein.
More detailed understanding of the exact molecular mechanism of action of Rex will allow for better design of therapeutic drugs against Rex function and ultimately HTLV replication. Expand
PDZ binding motif of HTLV-1 Tax promotes virus-mediated T-cell proliferation in vitro and persistence in vivo.
The results provide the first direct evidence suggesting that PBM-mediated associations between Tax-1 and cellular proteins play a key role in HTLV-induced cell proliferation and genetic instability in vitro and facilitate viral persistence in vivo. Expand
RNA helicase A interacts with divergent lymphotropic retroviruses and promotes translation of human T-cell leukemia virus type 1
- Cheryl Bolinger, Alper Yilmaz, +6 authors K. Boris-Lawrie
- Medicine, Biology
- Nucleic acids research
- 1 April 2007
It is concluded that PCE/RHA is an important translation regulatory axis of multiple lymphotropic retroviruses that have evolved a convergent RNA–protein interaction to modulate translation of their highly structured mRNA. Expand