ArticleMolecular and cellular biology2016
Protein Kinase C-Mediated Phosphorylation of BCL11B at Serine 2 Negatively Regulates Its Interaction with NuRD Complexes during CD4+ T-Cell Activation.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Trial
- Bcl11b dose-dependently regulates positive selection of CD8 T cells to the virtual memory fate.bioRxiv : the preprint server for biology · 2026Article
- Bipartite DNA binding domain of transcription factor BCL11B binds clustered short DNA sequence motifs.bioRxiv : the preprint server for biology · 2026Article
- Analysis of the Transcriptional Control ofAnimals : an open access journal from MDPI · 2025Article
- Prognostic and immunological significance of metastasis-associated protein 3 in patients with thymic epithelial tumors.Discover oncology · 2024Article
- The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.Nucleic acids research · 2024Article
- BCL11B and the NuRD complex cooperatively guard T-cell fate and inhibit OPA1-mediated mitochondrial fusion in T cells.The EMBO journal · 2023Article
- BCL11B depletion induces the development of highly cytotoxic innate T cells out of IL-15 stimulated peripheral blood αβ CD8+ T cells.Oncoimmunology · 2022Article
- Two types of immune infiltrating cells and six hub genes can predict the occurrence of myasthenia gravis in patients with thymoma.Bioengineered · 2021Article
- Viruses, SUMO, and immunity: the interplay between viruses and the host SUMOylation system.Journal of neurovirology · 2021Review
- Histone H3 N-terminal mimicry drives a novel network of methyl-effector interactions.The Biochemical journal · 2021Article
- Unveiling the N-Terminal Homodimerization of BCL11B by Hybrid Solvent Replica-Exchange Simulations.International journal of molecular sciences · 2021Article
- Ush regulates hemocyte-specific gene expression, fatty acid metabolism and cell cycle progression and cooperates with dNuRD to orchestrate hematopoiesis.PLoS genetics · 2021Article
- Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies.Signal transduction and targeted therapy · 2021Review
- Epigenetic Dynamics in the Function of T-Lineage Regulatory Factor Bcl11b.Frontiers in immunology · 2021Review
- Article
- Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020Review
- Bcl11 Transcription Factors Regulate Cortical Development and Function.Frontiers in molecular neuroscience · 2020Review
- HIV-1 Vpr mediates the depletion of the cellular repressor CTIP2 to counteract viral gene silencing.Scientific reports · 2019Article
- A de novo substitution in BCL11B leads to loss of interaction with transcriptional complexes and craniosynostosis.Human molecular genetics · 2019Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor BCL11B/CTIP2 is a major regulatory protein implicated in various aspects of development, function and survival of T cells. Mitogen-activated protein kinase (MAPK)-mediated phosphorylation and SUMOylation modulate BCL11B transcriptional activity, switching it from a repressor in naive murine thymocytes to a transcriptional activator in activated thymocytes. Here, we show that BCL11B interacts via its conserved N-terminal MSRRKQ motif with endogenous MTA1 and MTA3 proteins to recruit various NuRD complexes. Furthermore, we demonstrate that protein kinase C (PKC)-mediated phosphorylation of BCL11B Ser2 does not significantly impact BCL11B SUMOylation but negatively regulates NuRD recruitment by dampening the interaction with MTA1 or MTA3 (MTA1/3) and RbAp46 proteins. We detected increased phosphorylation of BCL11B Ser2 upon in vivo activation of transformed and primary human CD4(+) T cells. We show that following activation of CD4(+) T cells, BCL11B still binds to IL-2 and Id2 promoters but activates their transcription by recruiting P300 instead of MTA1. Prolonged stimulation results in the direct transcriptional repression of BCL11B by KLF4. Our results unveil Ser2 phosphorylation as a new BCL11B posttranslational modification linking PKC signaling pathway to T-cell receptor (TCR) activation and define a simple model for the functional switch of BCL11B from a transcriptional repressor to an activator during TCR activation of human CD4(+) T cells.
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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.