ArticleMolecular and cellular biology2012
Androgen-induced activation of gonadotropin-regulated testicular RNA helicase (GRTH/Ddx25) transcription: essential role of a nonclassical androgen response element half-site.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- What Does Androgen Receptor Signaling Pathway in Sertoli Cells During Normal Spermatogenesis Tell Us?Frontiers in endocrinology · 2022Review
- Blockade of GRTH/DDX25 Phosphorylation by Cyclic Peptides Provides an Avenue for Developing a Nonhormonal Male Contraceptive.Journal of medicinal chemistry · 2021Article
- Linking Phospho-Gonadotropin Regulated Testicular RNA Helicase (GRTH/DDX25) to Histone Ubiquitination and Acetylation Essential for Spermatid Development During Spermiogenesis.Frontiers in cell and developmental biology · 2020Article
- Targeted knock-in mice with a human mutation in GRTH/DDX25 reveals the essential role of phosphorylated GRTH in spermatid development during spermatogenesis.Human molecular genetics · 2019Article
- Characterization of the Phosphorylation Site of GRTH/DDX25 and Protein Kinase A Binding Interface Provides Structural Basis for the Design of a Non-Hormonal Male Contraceptive.Scientific reports · 2019Article
- Gonadotropin Regulation Testicular RNA Helicase, Two Decades of Studies on Its Structure Function and Regulation From Its Discovery Opens a Window for Development of a Non-hormonal Oral Male Contraceptive.Frontiers in endocrinology · 2019Review
- Germ Cell Nuclear Factor (GCNF/RTR) Regulates Transcription of Gonadotropin-Regulated Testicular RNA Helicase (GRTH/DDX25) in Testicular Germ Cells--The Androgen Connection.Molecular endocrinology (Baltimore, Md.) · 2015Article
- A 5'-flanking region of gonadotropin-regulated testicular RNA helicase (GRTH/DDX25) gene directs its cell-specific androgen-regulated gene expression in testicular germ cells.Endocrinology · 2013Article
- GRTH: a key to understanding androgen-mediated germ cell signaling.Endocrinology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
GRTH, a testis-specific member of the DEAD-box family of RNA helicases essential for spermatogenesis, is present in Leydig cells (LC) and germ cells. In LC, it exerts an autocrine negative regulation on androgen production induced by gonadotropin. GRTH is transcriptionally upregulated by gonadotropin via cyclic AMP/androgen through androgen receptors (AR). For studies of GRTH regulation by androgen in LC, we utilized in vitro/in vivo models. Androgen-induced GRTH expression was prevented by an AR antagonist. Two putative atypical ARE half-sites are present at bp -200 and -827 (ARE1 and ARE2). Point mutation of ARE2 prevented androgen-induced AR binding/function and upregulation of GRTH transcription. Chromatin immunoprecipitation (ChIP) assays showed recruitment of AR, SRC-1, Med-1, transcription factor IIB (TFIIB), and polymerase II (PolII) to GRTH ARE2 (bp -980/-702) and to the promoter region (bp -80/+63). ChIP3C assays revealed short-range chromosomal looping between AR/ARE2 and the core transcriptional machinery at the promoter. Knockdown of Med-1 and/or SRC-1 demonstrated the presence of a nonproductive complex which included AR, TFIIB, and PolII and the essential role of these coactivators in the transcriptional activation of GRTH. Our findings provide new insights into the molecular mechanism of androgen-regulated transcription in LC.
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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.