ArticlePloS one2009
The TCL1A oncoprotein interacts directly with the NF-kappaB inhibitor IkappaB.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Comparative transcriptomic meta-analysis reveals elevated TCL1A expression in human circulating immune cells across chronic pain conditions.British journal of anaesthesia · 2026Pooled it
- Molecular basis for the inhibition of de novo DNA methylation by TCL1A.Nature communications · 2026Article
- Review
- Constitutive activation of Lyn kinase enhances BCR responsiveness, but not the development of CLL in Eµ-TCL1 mice.Blood advances · 2020Article
- Two high-risk susceptibility loci at 6p25.3 and 14q32.13 for Waldenström macroglobulinemia.Nature communications · 2018Article
- T-Cell Leukemia/Lymphoma 1 (TCL1): An Oncogene Regulating Multiple Signaling Pathways.Frontiers in oncology · 2018Article
- Organometallic nucleosides induce non-classical leukemic cell death that is mitochondrial-ROS dependent and facilitated by TCL1-oncogene burden.Molecular cancer · 2015Article
- Article
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Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The T cell leukaemia/lymphoma 1A (TCL1A) oncoprotein plays key roles in several B and T cell malignancies. Lacking enzymatic activity, TCL1A's transforming action was linked to its capacity to co-activate the protein kinase AKT via binding to its pleckstrin homology (PH) domain. However, perturbation of AKT signalling alone was recently shown insufficient to explain TCL1A oncogenesis, suggesting that TCL1A has additional cellular partners. Searching for such additional targets, we found that TCL1A binds specifically and directly to the ankyrin domain of IkappaB, the inhibitor of the NF-kappaB transcription factors. Through binding assays and a structural analysis by small angle X-ray scattering, we show that TCL1A and IkappaB interact in yeast-two-hybrid systems, when transiently overexpressed in 293 cells, and as recombinant proteins in vitro. We further establish that the association between TCL1A and IkappaB is compatible with AKT binding to TCL1A, but incompatible with IkappaB binding to NF-kappaB. By interfering with the inhibition of NF-kappaB by IkappaB, TCL1A may increase the concentration of free NF-kappaB molecules sufficiently to trigger expression of anti-apoptotic genes. Thus our data suggest an additional route by which TCL1A might cause cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.