ArticleMolecular and cellular biology2001
JAK2 activates TFII-I and regulates its interaction with extracellular signal-regulated kinase.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- An assessment of gene-by-gene interactions as a tool to unfold missing heritability in dyslexia.Human genetics · 2015Trial
- Case Report: Molecular diagnostics and clinical courses of two adult spinal pilocytic astrocytoma long-term survivors with GTF2I::BRAF fusion.Frontiers in oncology · 2026Article
- Article
- The contribution of GTF2I haploinsufficiency to Williams syndrome.Molecular and cellular probes · 2018Review
- Cross-talk between endoplasmic reticulum (ER) stress and the MEK/ERK pathway potentiates apoptosis in human triple negative breast carcinoma cells: role of a dihydropyrimidone, nifetepimine.The Journal of biological chemistry · 2015Article
- A theoretical molecular network for dyslexia: integrating available genetic findings.Molecular psychiatry · 2011Review
- 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
- Induction of chromosomally integrated HIV-1 LTR requires RBF-2 (USF/TFII-I) and Ras/MAPK signaling.Virus genes · 2007Article
- Solution structure of the general transcription factor 2I domain in mouse TFII-I protein.Protein science : a publication of the Protein Society · 2007Article
- Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I.Molecular and cellular biology · 2006Article
- Phosphoproteome profiling of transforming growth factor (TGF)-beta signaling: abrogation of TGFbeta1-dependent phosphorylation of transcription factor-II-I (TFII-I) enhances cooperation of TFII-I and Smad3 in transcription.Molecular biology of the cell · 2005Article
- TFII-I regulates induction of chromosomally integrated human immunodeficiency virus type 1 long terminal repeat in cooperation with USF.Journal of virology · 2005Article
- Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor Bright.Molecular and cellular biology · 2005Article
- Comparison of TFII-I gene family members deleted in Williams-Beuren syndrome.Protein science : a publication of the Protein Society · 2004Article
- Signal transducer and activator of transcription (Stat) 5 controls the proliferation and differentiation of mammary alveolar epithelium.The Journal of cell biology · 2001Article
- 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
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
TFII-I is a transcription factor that shuttles between the cytoplasm and nucleus and is regulated by serine and tyrosine phosphorylation. Tyrosine phosphorylation of TFII-I can be regulated in a signal-dependent manner in various cell types. In B lymphocytes, Bruton's tyrosine kinase has been identified as a TFII-I tyrosine kinase. Here we report that JAK2 can phosphorylate and regulate TFII-I in nonlymphoid cells. The activity of TFII-I on the c-fos promoter in response to serum can be abolished by dominant negative JAK2 or the specific JAK2 kinase inhibitor AG490. Consistent with this, we have also found that JAK2 is activated by serum stimulation of fibroblasts. Tyrosine 248 of TFII-I is phosphorylated in vivo upon serum stimulation or JAK2 overexpression, and mutation of tyrosine 248 to phenylalanine inhibits the ability of JAK2 to phosphorylate TFII-I in vitro. Tyrosine 248 of TFII-I is required for its interaction with and phosphorylation by ERK and its in vivo activity on the c-fos promoter. These results indicate that the interaction between TFII-I and ERK, which is essential for its activity, can be regulated by JAK2 through phosphorylation of TFII-I at tyrosine 248. Thus, like the STAT factors, TFII-I is a direct substrate of JAK2 and a signal-dependent transcription factor that integrates signals from both tyrosine kinase and mitogen-activated protein kinase pathways to regulate transcription.
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Registered trials
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