The TOE1 gene was discovered as a target of the Egr1 transcription factor that participates in cell growth regulation through the upregulation of p21 and a cell cycle delay at the G2/M phase. We report here that TOE1 is able to bind to the p53 tumor suppressor protein, specifically interacting with the C terminal tetramerization domain of p53. We have further characterized this interaction through determination of binding kinetics using nanoporous optical interferometry and demonstrated that this interaction is capable of enhancing the transcriptional activity of p53-dependent gene targets. These results suggest a mechanistic role for TOE1 as a co-regulator of p53.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.febslet.2009.06.004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Genetic Analysis of Intraductal Carcinoma of the Prostate Detected in High-Grade Prostatic Intraepithelial Neoplasia Cases.
Cureus
December 2024
Department of Urology, Ehime University Graduate School of Medicine, Toon, JPN.
Background The accurate diagnosis of intraductal carcinoma of the prostate (IDC-P) is occasionally challenging due to the similarity in pathological morphology between IDC-P and high-grade prostatic intraepithelial neoplasia (HGPIN). In this report, we reviewed the pathology of cases previously diagnosed as HGPIN to search for IDC-P cases effectively. In addition, we examined whether those cases had genetic abnormalities.
View Article and Find Full Text PDFExome Sequencing Identified Susceptible Genes for High Residual Risks in Early-Onset Coronary Atherosclerotic Disease.
Clin Cardiol
December 2024
Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, P.R. China.
Aims: Despite the tremendous improvement in therapeutic medication and intervention for coronary atherosclerotic disease (CAD), residual risks remain. Exome sequencing enables identification of rare variants and susceptibility genes for residual risks of early-onset coronary atherosclerotic disease (EOCAD) with well-controlled conventional risk factors.
Methods: We performed whole-exome sequencing of subjects who had no conventional risk factors, defined as higher body mass index, smoking, hypertension and dyslipidemia, screened from 1950 patients with EOCAD (age ≤ 45 years, at least 50% stenosis of coronary artery by angiography), and selected control subjects from 1006 elder (age ≥ 65 years) with < 30% coronary stenosis.
TOE1 deadenylase inhibits gastric cancer cell proliferation by regulating cell cycle progression.
Biochim Biophys Acta Gen Subj
January 2025
Beijing International Science and Technology Cooperation Base of Antivirus Drug, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, China. Electronic address:
TOE1, also known as hCaf1z, belongs to the DEDD superfamily of deadenylases and a newly identified isoenzyme of hCaf1 deadenylases. Previous research has demonstrated that TOE1 has deadenylase activity, which can catalyze the degradation of poly(A) substrates and interact with hCcr4d to form the unconventional human Ccr4-Caf1 deadenylase complex. Our recent research indicates that hCaf1a and hCaf1b isoenzymes, highly expressed in gastric cancer, promote gastric cancer cell proliferation and tumorigenicity via modulating cell cycle progression.
View Article and Find Full Text PDFNovel heterozygous missense variants in the gene linked to pontocerebellar hypoplasia type 7.
Genes Dis
January 2025
Jining Medical University, Jining, Shandong 272067, China.
Toe1 promotes proliferation and differentiation of neural progenitor cells.
Heliyon
October 2024
Shenzhen Key Laboratory of Nanozymes and Translational Cancer Research, Department of Otolaryngology, Shenzhen Institute of Translational Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, 518035, China.
Toe1 (target of EGR1, member 1) is a 3'- exonuclease in the deadenylase family, essential for the maturation of small nuclear RNAs. Mutations in Toe1 are linked to pontocerebellar hypoplasia 7 (PCH7), a severe neurodegenerative syndrome affecting infants, characterized by progressive neurodegeneration, developmental delay, and genital abnormalities. The pathogenic mechanisms of PCH7 are unclear but are thought to involve abnormal neural stem cell (NSC) development during embryogenesis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!