ArticleNeurobiology of disease2008
Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease.
Article in Neurobiology of disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 61 citations in OpenAlex.
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- Genetic Inactivation of the Serotonin Transporter Dysregulates Expression of Neurotransmission Genes and Genome-Wide DNA Methylation Levels in the Medial Prefrontal Cortex of Male Rats During Postnatal Development.Developmental neurobiology · 2025Article
- INSTINCT: Multi-sample integration of spatial chromatin accessibility sequencing data via stochastic domain translation.Nature communications · 2025Article
- CNPY2 protects against ER stress and is expressed by corticostriatal neurons together with CTIP2 in a mouse model of Huntington's disease.Frontiers in molecular neuroscience · 2024Article
- Dysfunction of cAMP-Protein Kinase A-Calcium Signaling Axis in Striatal Medium Spiny Neurons: A Role in Schizophrenia and Huntington's Disease Neuropathology.Biological psychiatry global open science · 2023Article
- Postnatal Conditional Deletion ofBiomedicines · 2022Article
- Mutant Huntingtin Protein Interaction Map Implicates Dysregulation of Multiple Cellular Pathways in Neurodegeneration of Huntington's Disease.Journal of Huntington's disease · 2022Article
- The Prevailing Role of Topoisomerase 2 Beta and its Associated Genes in Neurons.Molecular neurobiology · 2021Review
- HIV-1 persistence in the CNS: Mechanisms of latency, pathogenesis and an update on eradication strategies.Virus research · 2021Review
- Epigenetic Dynamics in the Function of T-Lineage Regulatory Factor Bcl11b.Frontiers in immunology · 2021Review
- Quantification of Huntington's Disease Related Markers in the R6/2 Mouse Model.Frontiers in molecular neuroscience · 2020Article
- Bcl11 Transcription Factors Regulate Cortical Development and Function.Frontiers in molecular neuroscience · 2020Review
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- CTIP2-Regulated Reduction in PKA-Dependent DARPP32 Phosphorylation in Human Medium Spiny Neurons: Implications for Huntington Disease.Stem cell reports · 2019Article
- Faulty neuronal determination and cell polarization are reverted by modulating HD early phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mutant huntingtin induces iron overload via up-regulating IRP1 in Huntington's disease.Cell & bioscience · 2018Article
- Stability and Function of Hippocampal Mossy Fiber Synapses Depend onFrontiers in molecular neuroscience · 2018Article
- Function of B-Cell CLL/Lymphoma 11B in Glial Progenitor Proliferation and Oligodendrocyte Maturation.Frontiers in molecular neuroscience · 2018Article
- Reduced Expression of Foxp1 as a Contributing Factor in Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Bcl11b-A Critical Neurodevelopmental Transcription Factor-Roles in Health and Disease.Frontiers in cellular neuroscience · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Transcriptional dysregulation has emerged as a central pathogenic mechanism in Huntington's disease (HD), which is associated with neuropathological changes predominantly in the striatum. Here we demonstrate that expression of Bcl11b (a.k.a. CTIP2), a transcription factor exhibiting highly-enriched localization in adult striatum, is significantly decreased in HD cells, mouse models and human subjects and that overexpression of Bcl11b attenuates toxic effects of mutant huntingtin in cultured striatal neurons. We show that Bcl11b directly activates the proximal promoter regions of striatal-enriched genes and can increase mRNA levels of striatal-expressing genes. We further demonstrate an interaction between Bcl11b and huntingtin protein in cultured cells and brain homogenates from HD R6/1 and YAC72 transgenic mice. We propose that sequestration and/or decreased expression of Bcl11b in HD is responsible, at least in part, for the dysregulation of striatal gene expression observed in HD and may contribute to the specificity of pathology observed in this disease.
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