ArticleNucleic acids research2010
Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylation.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Retraction of 'Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylation'.Nucleic acids research · 2021Article
- Chemical Decorations of "MARs" Residents in Orchestrating Eukaryotic Gene Regulation.Frontiers in cell and developmental biology · 2020Review
- Interactomic analysis of REST/NRSF and implications of its functional links with the transcription suppressor TRIM28 during neuronal differentiation.Scientific reports · 2016Article
- The lectin-binding pattern of nucleolin and its interaction with endogenous galectin-3.Cellular & molecular biology letters · 2014Article
- RNA-binding protein nucleolin in disease.RNA biology · 2012Review
- Article
Corrections and comments
- Correction · 2013-11-27Falsification/Fabrication of Image · Investigation by Journal/Publisher · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/D99D6839FD571DF8F90B444BE05F2B;
- Retraction · 2021-11-17Falsification/Fabrication of Image · Investigation by Journal/Publisher · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/D99D6839FD571DF8F90B444BE05F2B;
- Erratum issued
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Non-malignant cells can be transformed via the activation of kinases that control degradation of neural-restrictive silencer factor (REST). Here, we identify a mechanism that contributes to the activation of genes, expression of which is controlled by responsive elements containing overlapping binding sites for REST and nucleolin. We demonstrate that both phosphorylated and non-phosphorylated nucleolin-bound DNA; however, only phosphorylated nucleolin successfully competed with either full-length REST or a REST-derived DNA-binding peptide, REST68, for binding to the overlapping binding sites. We show that this interplay between the two transcription factors regulates the activation of cell survival and immunomodulatory genes in tumors and non-malignant cells with activated protein kinase C, which is accompanied with alterations in cell proliferation and apoptosis. We propose a model for the regulation of these genes, which brings a new insight into the molecular mechanisms that control cellular transformation driven by activation of protein kinases.
Indexed as
Identifiers
What OpenQuestion holds
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.