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The HTLV-1 Tax interactome.

Boxus M, Twizere JC, Legros S, Dewulf JF, Kettmann R, Willems L - Retrovirology (2008)

Bottom Line: Tax1 affects a wide variety of cellular signalling pathways leading to transcriptional activation, proliferation and ultimately transformation.To carry out these functions, Tax1 interacts with and modulates activity of a number of cellular proteins.In this review, we summarize the present knowledge of the Tax1 interactome and propose a rationale for the broad range of cellular proteins identified so far.

View Article: PubMed Central - HTML - PubMed

Affiliation: University Academia Wallonie-Europe, Molecular and Cellular Biology at FUSAGx, Gembloux, Belgium. boxus.m@fsagx.ac.be

ABSTRACT
The Tax1 oncoprotein encoded by Human T-lymphotropic virus type I is a major determinant of viral persistence and pathogenesis. Tax1 affects a wide variety of cellular signalling pathways leading to transcriptional activation, proliferation and ultimately transformation. To carry out these functions, Tax1 interacts with and modulates activity of a number of cellular proteins. In this review, we summarize the present knowledge of the Tax1 interactome and propose a rationale for the broad range of cellular proteins identified so far.

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Related in: MedlinePlus

Effect of Tax1 on cell cycle progression. Through a series of interactions with cell-cycle associated proteins, Tax1 accelerates G1/S transition (A), attenuates Chk1/2 activity (B), induces supernumerary centrosomes and impedes SAC (spindle assembly checkpoint) activity (C).
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Figure 3: Effect of Tax1 on cell cycle progression. Through a series of interactions with cell-cycle associated proteins, Tax1 accelerates G1/S transition (A), attenuates Chk1/2 activity (B), induces supernumerary centrosomes and impedes SAC (spindle assembly checkpoint) activity (C).

Mentions: Cell cycle progression is a tightly regulated process controlled by cyclins associated with cyclin-dependent kinases (CDK). Cyclins D and E cooperate with CDK4/6 and CDK2 to mediate passage through G1 phase and G1/S transition, respectively [218]. Cyclin D-CDK4/6 and Cyclin E-CDK2 complexes target the Rb retinoblastoma protein (Figure 3). In its hypophosphorylated form, Rb is bound to the transcription factor E2F1, and upon phosphorylation, Rb frees E2F1, which activates transcription of genes required for transition from G1 to S. G1/S progression can be inhibited by CDK inhibitors (CDKI) such as p15INK4b, p16INK4a, p18INK4c and p19INK4d by preventing cyclin D/CDK4/6 complex formation. Tax1 reprograms cell cycle progression, particularly at G1/S transition, through different mechanisms pertaining to transcriptional activation or repression, post-translational modifications and protein-protein interactions [219,220].


The HTLV-1 Tax interactome.

Boxus M, Twizere JC, Legros S, Dewulf JF, Kettmann R, Willems L - Retrovirology (2008)

Effect of Tax1 on cell cycle progression. Through a series of interactions with cell-cycle associated proteins, Tax1 accelerates G1/S transition (A), attenuates Chk1/2 activity (B), induces supernumerary centrosomes and impedes SAC (spindle assembly checkpoint) activity (C).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2533353&req=5

Figure 3: Effect of Tax1 on cell cycle progression. Through a series of interactions with cell-cycle associated proteins, Tax1 accelerates G1/S transition (A), attenuates Chk1/2 activity (B), induces supernumerary centrosomes and impedes SAC (spindle assembly checkpoint) activity (C).
Mentions: Cell cycle progression is a tightly regulated process controlled by cyclins associated with cyclin-dependent kinases (CDK). Cyclins D and E cooperate with CDK4/6 and CDK2 to mediate passage through G1 phase and G1/S transition, respectively [218]. Cyclin D-CDK4/6 and Cyclin E-CDK2 complexes target the Rb retinoblastoma protein (Figure 3). In its hypophosphorylated form, Rb is bound to the transcription factor E2F1, and upon phosphorylation, Rb frees E2F1, which activates transcription of genes required for transition from G1 to S. G1/S progression can be inhibited by CDK inhibitors (CDKI) such as p15INK4b, p16INK4a, p18INK4c and p19INK4d by preventing cyclin D/CDK4/6 complex formation. Tax1 reprograms cell cycle progression, particularly at G1/S transition, through different mechanisms pertaining to transcriptional activation or repression, post-translational modifications and protein-protein interactions [219,220].

Bottom Line: Tax1 affects a wide variety of cellular signalling pathways leading to transcriptional activation, proliferation and ultimately transformation.To carry out these functions, Tax1 interacts with and modulates activity of a number of cellular proteins.In this review, we summarize the present knowledge of the Tax1 interactome and propose a rationale for the broad range of cellular proteins identified so far.

View Article: PubMed Central - HTML - PubMed

Affiliation: University Academia Wallonie-Europe, Molecular and Cellular Biology at FUSAGx, Gembloux, Belgium. boxus.m@fsagx.ac.be

ABSTRACT
The Tax1 oncoprotein encoded by Human T-lymphotropic virus type I is a major determinant of viral persistence and pathogenesis. Tax1 affects a wide variety of cellular signalling pathways leading to transcriptional activation, proliferation and ultimately transformation. To carry out these functions, Tax1 interacts with and modulates activity of a number of cellular proteins. In this review, we summarize the present knowledge of the Tax1 interactome and propose a rationale for the broad range of cellular proteins identified so far.

Show MeSH
Related in: MedlinePlus