ArticleRetrovirology2004
Two discrete events, human T-cell leukemia virus type I Tax oncoprotein expression and a separate stress stimulus, are required for induction of apoptosis in T-cells.
Article in Retrovirology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Tax-1 and Tax-2 similarities and differences: focus on post-translational modifications and NF-κB activation.Frontiers in microbiology · 2013Article
- Article
- How the DNA damage response determines the fate of HTLV-1 Tax-expressing cells.Retrovirology · 2012Article
- The human T-cell leukemia virus type 1 oncoprotein tax controls forkhead box O4 activity through degradation by the proteasome.Journal of virology · 2011Article
- Hematopoietic stem cells and retroviral infection.Retrovirology · 2010Review
- The HTLV-1 Tax interactome.Retrovirology · 2008Review
- Proinflammatory cytokine gene induction by human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 Tax in primary human glial cells.Journal of virology · 2007Article
- Quantification of the virus-host interaction in human T lymphotropic virus I infection.Retrovirology · 2005Article
- Induction of cell cycle arrest by human T-cell lymphotropic virus type 1 Tax in hematopoietic progenitor (CD34+) cells: modulation of p21cip1/waf1 and p27kip1 expression.Journal of virology · 2005Article
- Review
- Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity.Retrovirology · 2004Review
- Specific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex.Retrovirology · 2004Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIt is poorly understood why many transforming proteins reportedly enhance both cell growth (transformation) and cell death (apoptosis). At first glance, the ability to transform and the ability to engender apoptosis seem to be contradictory. Interestingly, both abilities have been widely reported in the literature for the HTLV-I Tax protein.
resultsTo reconcile these apparently divergent findings, we sought to understand how Tax might cause apoptosis in a Jurkat T-cell line, JPX-9. Tax expression can be induced equally by either cadmium (Cd) or zinc (Zn) in JPX-9 cells. Surprisingly, when induced by Zn, but not when induced by Cd, Tax-expression produced significant apoptosis. Under our experimental conditions, Zn but not Cd, induced SAPK (stress activated protein kinase)/JNK (Jun kinase) activation in cells. We further showed that transient over-expression of Tax-alone or Jun-alone did not induce cell death. On the other hand, co-expression of Tax plus Jun did effectively result in apoptosis.
conclusionWe propose that Tax-expression alone in a T-cell background insufficiently accounts for apoptosis. On the other hand, Tax plus activation of a stress kinase can induce cell death. Thus, HTLV-I infection/transformation of cells requires two discrete events (i.e. oncoprotein expression and stress) to produce apoptosis.
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Registered trials
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