ArticleMolecular and cellular biology2005
FOXC1 transcriptional regulatory activity is impaired by PBX1 in a filamin A-mediated manner.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Article
- FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid.International journal of molecular sciences · 2021Article
- Structural basis for DNA recognition by FOXC2.Nucleic acids research · 2019Article
- An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer.eLife · 2018Article
- Skeletal Dysplasia Mutations Effect on Human Filamins' Structure and Mechanosensing.Scientific reports · 2017Article
- FoxC1 promotes epithelial-mesenchymal transition through PBX1 dependent transactivation of ZEB2 in esophageal cancer.American journal of cancer research · 2017Article
- Cytoskeletal Filamin A Differentially Modulates RNA Polymerase III Gene Transcription in Transformed Cell Lines.The Journal of biological chemistry · 2016Article
- Introducing STRaNDs: shuttling transcriptional regulators that are non-DNA binding.Nature reviews. Molecular cell biology · 2016Review
- Unravelling a new mechanism linking actin polymerization and gene transcription.Nucleus (Austin, Tex.) · 2016Review
- Survivin modulates genes with divergent molecular functions and regulates proliferation of hematopoietic stem cells through Evi-1.Leukemia · 2015Article
- Whole exome sequence analysis of Peters anomaly.Human genetics · 2014Article
- Hypoxia-induced and calpain-dependent cleavage of filamin A regulates the hypoxic response.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Biochemistry of the tale transcription factors PREP, MEIS, and PBX in vertebrates.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Review
- The dual role of filamin A in cancer: can't live with (too much of) it, can't live without it.Endocrine-related cancer · 2013Review
- Monoubiquitination of filamin B regulates vascular endothelial growth factor-mediated trafficking of histone deacetylase 7.Molecular and cellular biology · 2013Article
- Cytoskeletal protein filamin A is a nucleolar protein that suppresses ribosomal RNA gene transcription.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Filamin A-hinge region 1-EGFP: a novel tool for tracking the cellular functions of filamin A in real-time.PloS one · 2012Article
- Mutations in the N-terminal actin-binding domain of filamin C cause a distal myopathy.American journal of human genetics · 2011Article
- Pbx homeodomain proteins: TALEnted regulators of limb patterning and outgrowth.Developmental dynamics : an official publication of the American Association of Anatomists · 2011Review
- Cell type-specific filamin complex regulation by a novel class of HECT ubiquitin ligase is required for normal cell motility and patterning.Development (Cambridge, England) · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FOXC1 mutations underlie Axenfeld-Rieger syndrome, an autosomal dominant disorder that is characterized by a spectrum of ocular and nonocular phenotypes and results in an increased susceptibility to glaucoma. Proteins interacting with FOXC1 were identified in human nonpigmented ciliary epithelial cells. Here we demonstrate that FOXC1 interacts with the actin-binding protein filamin A (FLNA). In A7 melanoma cells possessing elevated levels of nuclear FLNA, FOXC1 is unable to activate transcription and is partitioned to an HP1alpha, heterochromatin-rich region of the nucleus. This inhibition is mediated through an interaction between FOXC1 and the homeodomain protein PBX1a. In addition, we demonstrate that efficient nuclear and subnuclear localization of PBX1 is mediated by FLNA. Together, these data reveal a mechanism by which structural proteins such as FLNA can influence the activity of a developmentally and pathologically important transcription factor such as FOXC1. Given the resemblance of the skeletal phenotypes caused by FOXC1 loss-of-function mutations and FLNA gain-of-function mutations, this inhibitory activity of FLNA on FOXC1 may contribute to the pathogenesis of FLNA-linked skeletal disorders.
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Registered trials
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