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Mechanisms of HTLV-1 transformation

Authors: Kylene, Kehn; Reem, Berro; Cynthia, de la Fuente; Katharine, Strouss; Elodie, Ghedin; Shabnam, Dadgar; Maria Elena, Bottazzi; +2 Authors

Mechanisms of HTLV-1 transformation

Abstract

HTLV-1 is the etiological agent of the fatal disease adult T-cell leukemia. The virus encodes many proteins including several accessory proteins, p12I, p13II, p27I, and p30II, whose roles have recently begun to be elucidated. These accessory proteins are important in T-cell activation, transcriptional regulation, viral persistence, and virus assembly. The viral oncogene Tax is thought to be largely responsible for tumorigenesis, although the precise mechanisms underlying transformation are not completely understood. Tax has a profound impact on transcription, cell growth regulation, genomic stability and apoptosis. This review will provide possible contributions of the accessory proteins to transformation as well as highlight the alterations of the above-mentioned cellular events by Tax. Animal models of both Tax and the accessory proteins are also included based on the essential information on the transformation process in vivo that they provide.

Related Organizations
Keywords

Gene Expression Regulation, Viral, Human T-lymphotropic virus 1, Leukemia, T-Cell, DNA Repair, Transcription, Genetic, Cell Cycle, Mitosis, Apoptosis, Gene Products, tax, Oncogene Proteins, Viral, Cell Transformation, Viral, Lymphocyte Activation, Virus Replication, Disease Models, Animal, Cell Transformation, Neoplastic, Animals, Humans, Viral Regulatory and Accessory Proteins, Cell Proliferation

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
17
Average
Average
Top 10%
Related to Research communities
Cancer Research
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