ArticleEuropean journal of immunology2009
Characterization of a novel interaction between transcription factor TFII-I and the inducible tyrosine kinase in T cells.
Article in European journal of immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- CRTAC1 inhibits progression of lung adenocarcinoma by suppressing integrin/FAK signaling.Oncogene · 2026Article
- Gtf2i-encoded transcription factor Tfii-i regulates myelination via Sox10 and Mbp regulatory elements.Nature communications · 2025Article
- Risk Allele rs117026326-Mediated Alternative Splicing of GTF2I Promotes B Cell Proliferation in Primary Sjögren's Syndrome.Journal of immunology research · 2025Article
- Association ofNeural regeneration research · 2019Article
- The contribution of GTF2I haploinsufficiency to Williams syndrome.Molecular and cellular probes · 2018Review
- Consistent hypersocial behavior in mice carrying a deletion ofBrain and behavior · 2018Article
- Pathophysiology of TFII-I: Old Guard Wearing New Hats.Trends in molecular medicine · 2017Review
- Identification and selective expansion of functionally superior T cells expressing chimeric antigen receptors.Journal of translational medicine · 2015Article
- Contribution of Genetic Factors to Sjögren's Syndrome and Sjögren's Syndrome Related Lymphomagenesis.Journal of immunology research · 2015Review
- Targeting Interleukin-2-Inducible T-cell Kinase (ITK) in T-Cell Related Diseases.Postdoc journal : a journal of postdoctoral research and postdoctoral affairs · 2014Article
- Evolution of general transcription factors.Journal of molecular evolution · 2013Article
- Review
- Role for transcription factor TFII-I in the suppression of SSeCKS/Gravin/Akap12 transcription by Src.International journal of cancer · 2011Article
- Itk: the rheostat of the T cell response.Journal of signal transduction · 2011Article
- T-cell signaling regulated by the Tec family kinase, Itk.Cold Spring Harbor perspectives in biology · 2010Review
- Improving development of the molecular signature for diagnosis of acute respiratory viral infections.Cell host & microbe · 2010Article
- IL-2-inducible T-cell kinase (ITK) finds another (dance) partner...TFII-I.European journal of immunology · 2009Article
- Binding of Gtf2i-β/δ transcription factors to the ARMS2 gene leads to increased circulating HTRA1 in AMD patients and in vitro.The Journal of biological chemistryArticle
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
TCR signaling leads to the activation of kinases such as inducible tyrosine kinase (Itk), a key regulatory protein in T-lymphocyte activation and function. The homolog of Itk in B cells is Bruton's tyrosine kinase, previously shown to bind and phosphorylate the transcription factor TFII-I. TFII-I plays major roles in transcription and signaling. Our purpose herein was twofold: first, to identify some of the molecular determinants involved in TFII-I activation downstream of receptor crosslinking in T cells and second, to uncover the existence of Itk-TFII-I signaling in T lymphocytes. We report for the first time that TFII-I is tyrosine phosphorylated upon TCR, TCR/CD43, and TCR/CD28 co-receptor engagement in human and/or murine T cells. We show that Itk physically interacts with TFII-I and potentiates TFII-I-driven c-fos transcription. We demonstrate that TFII-I is phosphorylated upon co-expression of WT, but not kinase-dead, or kinase-dead/R29C mutant Itk, suggesting these residues are important for TFII-I phosphorylation, presumably via an Itk-dependent mechanism. Structural analysis of TFII-I-Itk interactions revealed that the first 90 residues of TFII-I are dispensable for Itk binding. Mutations within Itk's kinase, pleckstrin-homology, and proline-rich regions did not abolish TFII-I-Itk binding. Our results provide an initial step in understanding the biological role of Itk-TFII-I signaling in T-cell function.
Indexed as
Identifiers
What OpenQuestion holds
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.