ArticleJournal of nucleic acids2010
Regulation of HuR by DNA Damage Response Kinases.
Article in Journal of nucleic acids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 71 citations in OpenAlex.
- Phosphorylation at the disordered N-end makes HuR accumulate and dimerize in the cytoplasm.Nucleic acids research · 2024Article
- Tackling the HuRdle of radioresistance: a radiation perspective on the RNA-binding protein HuR.Translational cancer research · 2023Article
- RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.Advanced drug delivery reviews · 2022Review
- ARPC1B promotes mesenchymal phenotype maintenance and radiotherapy resistance by blocking TRIM21-mediated degradation of IFI16 and HuR in glioma stem cells.Journal of experimental & clinical cancer research : CR · 2022Article
- A global analysis on the differential regulation of RNA binding proteins (RBPs) by TNF-α as potential modulators of metabolic syndromes.BBA advances · 2022Article
- AU-Rich Element RNA Binding Proteins: At the Crossroads of Post-Transcriptional Regulation and Genome Integrity.International journal of molecular sciences · 2021Review
- Review
- STAU2 protein level is controlled by caspases and the CHK1 pathway and regulates cell cycle progression in the non-transformed hTERT-RPE1 cells.BMC molecular and cell biology · 2021Article
- Ionizing Radiation and Translation Control: A Link to Radiation Hormesis?International journal of molecular sciences · 2020Review
- Transite: A Computational Motif-Based Analysis Platform That Identifies RNA-Binding Proteins Modulating Changes in Gene Expression.Cell reports · 2020Article
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- Article
- Review
- Uncovering the Role of RNA-Binding Proteins in Gene Expression in the Immune System.Frontiers in immunology · 2018Review
- Transcriptional and post-transcriptional regulation of the ionizing radiation response by ATM and p53.Scientific reports · 2017Article
- LZAP is a novel Wip1 binding partner and positive regulator of its phosphatase activity in vitro.Cell cycle (Georgetown, Tex.) · 2017Article
- Radiation-induced translational control of gene expression.Translation (Austin, Tex.) · 2017Review
- HUR protects NONO from degradation by mir320, which is induced by p53 upon UV irradiation.Oncotarget · 2016Article
- Inhibiting cytoplasmic accumulation of HuR synergizes genotoxic agents in urothelial carcinoma of the bladder.Oncotarget · 2016Article
- PKM2 uses control of HuR localization to regulate p27 and cell cycle progression in human glioblastoma cells.International journal of cancer · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
As many DNA-damaging conditions repress transcription, posttranscriptional processes critically influence gene expression during the genotoxic stress response. The RNA-binding protein HuR robustly influences gene expression following DNA damage. HuR function is controlled in two principal ways: (1) by mobilizing HuR from the nucleus to the cytoplasm, where it modulates the stability and translation of target mRNAs and (2) by altering its association with target mRNAs. Here, we review evidence that two main effectors of ataxia-telangiectasia-mutated/ATM- and Rad3-related (ATM/ATR), the checkpoint kinases Chk1 and Chk2, jointly influence HuR function. Chk1 affects HuR localization by phosphorylating (hence inactivating) Cdk1, a kinase that phosphorylates HuR and thereby blocks HuR's cytoplasmic export. Chk2 modulates HuR binding to target mRNAs by phosphorylating HuR's RNA-recognition motifs (RRM1 and RRM2). We discuss how HuR phosphorylation by kinases including Chk1/Cdk1 and Chk2 impacts upon gene expression patterns, cell proliferation, and survival following genotoxic injury.
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.