ArticleThe Journal of biological chemistry2010
Transcription elongation regulator 1 is a co-integrator of the cell fate determination factor Dachshund homolog 1.
Article in The Journal of biological chemistry, 2010. 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, 31 citations in OpenAlex.
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- The DACH1 gene is frequently deleted in prostate cancer, restrains prostatic intraepithelial neoplasia, decreases DNA damage repair, and predicts therapy responses.Research square · 2023Article
- Sequence-specific recognition of a coding segment of humanRSC advances · 2021Article
- DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.The Journal of clinical investigation · 2021Article
- Investigating the role of dachshund b in the development of the pancreatic islet in zebrafish.Journal of diabetes investigation · 2021Article
- BF175 inhibits endometrial carcinoma through SREBP-regulated metabolic pathways in vitro.Molecular and cellular endocrinology · 2021Article
- Dachshund Depletion Disrupts Mammary Gland Development and Diverts the Composition of the Mammary Gland Progenitor Pool.Stem cell reports · 2019Article
- Effect of DACH1 on proliferation and invasion of laryngeal squamous cell carcinoma.Head & face medicine · 2018Article
- The Homeotic Protein SIX3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.Theranostics · 2018Article
- The retinal determination gene network: from developmental regulator to cancer therapeutic target.Oncotarget · 2016Review
- DACH1 Expresison in Osteosarcoma and Its Relationship with Proliferation and Angiogenesis.The Indian journal of surgery · 2015Article
- Interplay of retinal determination gene network with TGF-β signaling pathway in epithelial-mesenchymal transition.Stem cell investigation · 2015Review
- Cell fate factor DACH1 represses YB-1-mediated oncogenic transcription and translation.Cancer research · 2014Article
- The Eyes Absent proteins in development and disease.Cellular and molecular life sciences : CMLS · 2013Review
- Tumor-suppressive effects of CDK8 in endometrial cancer cells.Cell cycle (Georgetown, Tex.) · 2013Article
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
DACH1 (Dachshund homolog 1) is a key component of the retinal determination gene network and regulates gene expression either indirectly as a co-integrator or through direct DNA binding. The current studies were conducted to understand, at a higher level of resolution, the mechanisms governing DACH1-mediated transcriptional repression via DNA sequence-specific binding. DACH1 repressed gene transcription driven by the DACH1-responsive element (DRE). Recent genome-wide ChIP-Seq analysis demonstrated DACH1 binding sites co-localized with Forkhead protein (FOX) binding sites. Herein, DACH1 repressed, whereas FOX proteins enhanced, both DRE and FOXA-responsive element-driven gene expression. Reduced DACH1 expression using a shRNA approach enhanced FOX protein activity. As DACH1 antagonized FOX target gene expression and attenuated FOX signaling, we sought to identify limiting co-integrator proteins governing DACH1 signaling. Proteomic analysis identified transcription elongation regulator 1 (TCERG1) as the transcriptional co-regulator of DACH1 activity. The FF2 domain of TCERG1 was required for DACH1 binding, and the deletion of FF2 abolished DACH1 trans-repression function. The carboxyl terminus of DACH1 was necessary and sufficient for TCERG1 binding. Thus, DACH1 represses gene transcription through direct DNA binding to the promoter region of target genes by recruiting the transcriptional co-regulator, TCERG1.
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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.