ArticleThe Journal of biological chemistry2013
Oligodendrocyte transcription factor 1 (Olig1) is a Smad cofactor involved in cell motility induced by transforming growth factor-β.
Article in The Journal of biological chemistry, 2013. 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, 24 citations in OpenAlex.
- TGF-β Enhances Doxorubicin Resistance and Anchorage-Independent Growth in Cancer Cells by Inducing ALDH1A1 Expression.Cancer science · 2025Article
- The Snail signaling branch downstream of the TGF-β/Smad3 pathway mediates Rho activation and subsequent stress fiber formation.The Journal of biological chemistry · 2024Article
- Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin.Current issues in molecular biology · 2022Review
- Endothelial-specific depletion of TGF-β signaling affects lymphatic function.Inflammation and regeneration · 2021Article
- Neural stem/precursor cells dynamically change their epigenetic landscape to differentially respond to BMP signaling for fate switching during brain development.Genes & development · 2021Article
- Impact of the Olig Family on Neurodevelopmental Disorders.Frontiers in neuroscience · 2021Review
- Transgenic Analyses in Drosophila Reveal That mCORL1 Is Functionally Distinct from mCORL2 and dCORL.G3 (Bethesda, Md.) · 2019Article
- A comparative analysis of Smad-responsive motifs identifies multiple regulatory inputs for TGF-β transcriptional activation.The Journal of biological chemistry · 2019Article
- Variability of Betweenness Centrality and Its Effect on Identifying Essential Genes.Bulletin of mathematical biology · 2019Article
- Phosphorylation status at Smad3 linker region modulates transforming growth factor-β-induced epithelial-mesenchymal transition and cancer progression.Cancer science · 2019Review
- Zoledronic acid suppresses transforming growth factor-β-induced fibrogenesis by human gingival fibroblasts.International journal of molecular medicine · 2016Article
- Epithelial-mesenchymal transition is regulated at post-transcriptional levels by transforming growth factor-β signaling during tumor progression.Cancer science · 2015Review
- miR-136 modulates TGF-β1-induced proliferation arrest by targeting PPP2R2A in keratinocytes.BioMed research international · 2015Article
- Epithelial splicing regulatory proteins 1 (ESRP1) and 2 (ESRP2) suppress cancer cell motility via different mechanisms.The Journal of biological chemistry · 2014Article
- Astrocytic TGF-β signaling limits inflammation and reduces neuronal damage during central nervous system Toxoplasma infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Meeting report - TGF-β superfamily: signaling in development and disease.Journal of cell science · 2013Article
- TGF-β-induced cell motility requires downregulation of ARHGAPs to sustain Rac1 activity.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor (TGF)-β plays crucial roles in embryonic development and adult tissue homeostasis by eliciting various cellular responses in target cells. TGF-β signaling is principally mediated through receptor-activated Smad proteins, which regulate expression of target genes in cooperation with other DNA-binding transcription factors (Smad cofactors). In this study, we found that the basic helix-loop-helix transcription factor Olig1 is a Smad cofactor involved in TGF-β-induced cell motility. Knockdown of Olig1 attenuated TGF-β-induced cell motility in chamber migration and wound healing assays. In contrast, Olig1 knockdown had no effect on bone morphogenetic protein-induced cell motility, TGF-β-induced cytostasis, or epithelial-mesenchymal transition. Furthermore, we observed that cooperation of Smad2/3 with Olig1 is regulated by a peptidyl-prolyl cis/trans-isomerase, Pin1. TGF-β-induced cell motility, induction of Olig1-regulated genes, and physical interaction between Smad2/3 and Olig1 were all inhibited after knockdown of Pin1, indicating a novel mode of regulation of Smad signaling. We also found that Olig1 interacts with the L3 loop of Smad3. Using a synthetic peptide corresponding to the L3 loop of Smad3, we succeeded in selectively inhibiting TGF-β-induced cell motility. These findings may lead to a new strategy for selective regulation of TGF-β-induced cellular responses.
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