ArticleMolecular biology of the cell2007
Cell fate determination factor DACH1 inhibits c-Jun-induced contact-independent growth.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 73 citations in OpenAlex.
- Mining Chemotherapy Resistance Related Genes in Breast Cancer to Construct a New Prognosis Prediction Model-Based on GEO Database and Real-World Study.Human mutation · 2026Article
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- Article
- An intellectual disability-related MED23 mutation dysregulates gene expression by altering chromatin conformation and enhancer activities.Nucleic acids research · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer.Cell death and differentiation · 2022Article
- DACH1 inhibits breast cancer cell invasion and metastasis by down-regulating the transcription of matrix metalloproteinase 9.Cell death discovery · 2021Article
- Transcriptional control of CBX5 by the RNA binding proteins RBMX and RBMXL1 maintains chromatin state in myeloid leukemia.Nature cancer · 2021Article
- DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.The Journal of clinical investigation · 2021Article
- Molecular Mechanisms of Metal Toxicity in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2021Review
- MicroRNA-362 negatively and positively regulates SMAD4 expression in TGF-β/SMAD signaling to suppress cell migration and invasion.International journal of medical sciences · 2021Article
- Article
- DACH1 suppresses epithelial to mesenchymal transition (EMT) through Notch1 pathway and reverses progestin resistance in endometrial carcinoma.Cancer medicine · 2019Article
- Effect of DACH1 on proliferation and invasion of laryngeal squamous cell carcinoma.Head & face medicine · 2018Article
- The regulation of cytokine signaling by retinal determination gene network pathway in cancer.OncoTargets and therapy · 2018Review
- The Homeotic Protein SIX3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.Theranostics · 2018Article
- DACH1 suppresses breast cancer as a negative regulator of CD44.Scientific reports · 2017Article
- Master regulators in development: Views from the Drosophila retinal determination and mammalian pluripotency gene networks.Developmental biology · 2017Review
- Decreased DACH1 expression in glomerulopathy is associated with disease progression and severity.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
The cell fate determination factor DACH1 plays a key role in cellular differentiation in metazoans. DACH1 is engaged in multiple context-dependent complexes that activate or repress transcription. DACH1 can be recruited to DNA via the Six1/Eya bipartite transcription (DNA binding/coactivator) complex. c-Jun is a critical component of the activator protein (AP)-1 transcription factor complex and can promote contact-independent growth. Herein, DACH1 inhibited c-Jun-induced DNA synthesis and cellular proliferation. Excision of c-Jun with Cre recombinase, in c-jun(f1/f1) 3T3 cells, abrogated DACH1-mediated inhibition of DNA synthesis. c-Jun expression rescued DACH1-mediated inhibition of cellular proliferation. DACH1 inhibited induction of c-Jun by physiological stimuli and repressed c-jun target genes (cyclin A, beta-PAK, and stathmin). DACH1 bound c-Jun and inhibited AP-1 transcriptional activity. c-jun and c-fos were transcriptionally repressed by DACH1, requiring the conserved N-terminal (dac and ski/sno [DS]) domain. c-fos transcriptional repression by DACH1 requires the SRF site of the c-fos promoter. DACH1 inhibited c-Jun transactivation through the delta domain of c-Jun. DACH1 coprecipitated the histone deacetylase proteins (HDAC1, HDAC2, and NCoR), providing a mechanism by which DACH1 represses c-Jun activity through the conserved delta domain. An oncogenic v-Jun deleted of the delta domain was resistant to DACH1 repression. Collectively, these studies demonstrate a novel mechanism by which DACH1 blocks c-Jun-mediated contact-independent growth through repressing the c-Jun delta domain.
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Registered trials
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.