ArticleMolecular and cellular biology1999
Regulation of nuclear localization and transcriptional activity of TFII-I by Bruton's tyrosine kinase.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 110 citations in OpenAlex.
- CRTAC1 inhibits progression of lung adenocarcinoma by suppressing integrin/FAK signaling.Oncogene · 2026Article
- Transcription factor TFII-I fine tunes innate properties of B lymphocytes.Frontiers in immunology · 2023Article
- Review
- Sjögren's syndrome-associated SNPs increase GTF2I expression in salivary gland cells to enhance inflammation development.International immunology · 2021Article
- TFII-I-mediated polymerase pausing antagonizes GLI2 induction by TGFβ.Nucleic acids research · 2020Article
- Characterization of Cerebellum-Specific Ribosomal DNA Epigenetic Modifications in Alzheimer's Disease: Should the Cerebellum Serve as a Control Tissue After All?Molecular neurobiology · 2020Article
- The contribution of GTF2I haploinsufficiency to Williams syndrome.Molecular and cellular probes · 2018Review
- Pathophysiology of TFII-I: Old Guard Wearing New Hats.Trends in molecular medicine · 2017Review
- Role of Splice Variants of Gtf2i, a Transcription Factor Localizing at Postsynaptic Sites, and Its Relation to Neuropsychiatric Diseases.International journal of molecular sciences · 2017Review
- Gtf2ird1-Dependent Mohawk Expression Regulates Mechanosensing Properties of the Tendon.Molecular and cellular biology · 2016Article
- Role of Bruton's tyrosine kinase inhibitors in HIV-1-infected cells.Journal of neurovirology · 2015Article
- Review
- Effective identification of Akt interacting proteins by two-step chemical crosslinking, co-immunoprecipitation and mass spectrometry.PloS one · 2013Article
- GTF2IRD2 from the Williams-Beuren critical region encodes a mobile-element-derived fusion protein that antagonizes the action of its related family members.Journal of cell science · 2012Article
- Review
- Direct interactions of OCA-B and TFII-I regulate immunoglobulin heavy-chain gene transcription by facilitating enhancer-promoter communication.Molecular cell · 2011Article
- IL-2-inducible T-cell kinase (ITK) finds another (dance) partner...TFII-I.European journal of immunology · 2009Article
- Characterization of a novel interaction between transcription factor TFII-I and the inducible tyrosine kinase in T cells.European journal of immunology · 2009Article
- Signalling of the BCR is regulated by a lipid rafts-localised transcription factor, Bright.The EMBO journal · 2009Article
- Transgenic mice expressing dominant-negative bright exhibit defects in B1 B cells.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Bruton's tyrosine kinase (Btk) is required for normal B-cell development, as defects in Btk lead to X-linked immunodeficiency (xid) in mice and X-linked agammaglobulinemia (XLA) in humans. Here we demonstrate a functional interaction between the multifunctional transcription factor TFII-I and Btk. Ectopic expression of wild-type Btk enhances TFII-I-mediated transcriptional activation and its tyrosine phosphorylation in transient-transfection assays. Mutation of Btk in either the PH domain (R28C, as in the murine xid mutation) or the kinase domain (K430E) compromises its ability to enhance both the tyrosine phosphorylation and the transcriptional activity of TFII-I. TFII-I associates constitutively in vivo with wild-type Btk and kinase-inactive Btk but not xid Btk. However, membrane immunoglobulin M cross-linking in B cells leads to dissociation of TFII-I from Btk. We further show that while TFII-I is found in both the nucleus and cytoplasm of wild-type and xid primary resting B cells, nuclear TFII-I is greater in xid B cells. Most strikingly, receptor cross-linking of wild-type (but not xid) B cells results in increased nuclear import of TFII-I. Taken together, these data suggest that although the PH domain of Btk is primarily responsible for its physical interaction with TFII-I, an intact kinase domain of Btk is required to enhance transcriptional activity of TFII-I in the nucleus. Thus, mutations impairing the physical and/or functional association between TFII-I and Btk may result in diminished TFII-I-dependent transcription and contribute to defective B-cell development and/or 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.