ArticleCell cycle (Georgetown, Tex.)2011
The DNA damage effector Chk1 kinase regulates Cdc14B nucleolar shuttling during cell cycle progression.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 20 citations in OpenAlex.
- FBL promotes cancer cell resistance to DNA damage and BRCA1 transcription via YBX1.EMBO reports · 2023Article
- TORC1 inactivation promotes APC/C-dependent mitotic slippage in yeast and human cells.iScience · 2022Article
- Review
- Article
- The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites.Nature communications · 2017Article
- Perturbations at the ribosomal genes loci are at the centre of cellular dysfunction and human disease.Cell & bioscience · 2014Review
- Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.Oncotarget · 2012Review
- Multiple protein kinases influence the redistribution of fission yeast Clp1/Cdc14 phosphatase upon genotoxic stress.Molecular biology of the cell · 2012Article
- The nucleolar detention pathway: A cellular strategy for regulating molecular networks.Cell cycle (Georgetown, Tex.) · 2012Article
- Cdc14b: a new player in aging.Aging · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chk1 is a critical effector of DNA damage checkpoints necessary for the maintenance of chromosome integrity during cell cycle progression. Here we report, that Chk1 co-localized with the nucleolar marker, fibrillarin in response to radiation-induced DNA damage in human cells. Interestingly, in vitro studies using GST pull down assays identified the dual-specificity serine/threonine nucleolar phosphatase Cdc14B as a Chk1 substrate. Furthermore, Chk1, but not a kinase-dead Chk1 control, was shown to phosphorylate Cdc14B using an in vitro kinase assay. Co-immunoprecipitation experiments using exogenous Cdc14B transfected into human cells confirmed the interaction of Cdc14B and Chk1 during cell cycle. In addition, reduction of Chk1 levels via siRNA or UCN-01 treatment demonstrated that Chk1 activation following DNA damage was required for Cdc14B export from the nucleolus. These studies have revealed a novel interplay between Chk1 kinase and Cdc14B phosphatase involving radiation-induced nucleolar shuttling to facilitate error-free cell cycle progression and prevent genomic instability.
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.