ArticleJournal of proteomics & bioinformatics2008
Integrated Bioinformatics for Radiation-Induced Pathway Analysis from Proteomics and Microarray Data.
Article in Journal of proteomics & bioinformatics, 2008. 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
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
10 citing papers in PubMed, 26 citations in OpenAlex.
- The Role of MiR-5094 as a Proliferation Suppressor during Cellular Radiation Response via Downregulating STAT5b.Journal of Cancer · 2020Article
- Effects of ionizing radiation on biological molecules--mechanisms of damage and emerging methods of detection.Antioxidants & redox signaling · 2014Review
- Differential expression of thymic DNA repair genes in low-dose-rate irradiated AKR/J mice.Journal of veterinary science · 2013Article
- Proteomic profiling of ATM kinase proficient and deficient cell lines upon blockage of proteasome activity.Journal of proteomics · 2012Article
- Progesterone and DNA damage encourage uterine cell proliferation and decidualization through up-regulating ribonucleotide reductase 2 expression during early pregnancy in mice.The Journal of biological chemistry · 2012Article
- Human fibroblasts for large-scale "omics" investigations of ATM gene function.Advances in experimental medicine and biology · 2011Article
- Proteomic analysis of pathways involved in estrogen-induced growth and apoptosis of breast cancer cells.PloS one · 2011Article
- Omics-based molecular target and biomarker identification.Methods in molecular biology (Clifton, N.J.) · 2011Article
- The role of mass spectrometry-based metabolomics in medical countermeasures against radiation.Mass spectrometry reviewsReview
- Using systems biology approaches to understand cardiac inflammation and extracellular matrix remodeling in the setting of myocardial infarction.Wiley interdisciplinary reviews. Systems biology and medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Functional analysis and interpretation of large-scale proteomics and gene expression data require effective use of bioinformatics tools and public knowledge resources coupled with expert-guided examination. An integrated bioinformatics approach was used to analyze cellular pathways in response to ionizing radiation. ATM, or ataxia-telangiectasia mutated , a serine-threonine protein kinase, plays critical roles in radiation responses, including cell cycle arrest and DNA repair. We analyzed radiation responsive pathways based on 2D-gel/MS proteomics and microarray gene expression data from fibroblasts expressing wild type or mutant ATM gene. The analysis showed that metabolism was significantly affected by radiation in an ATM dependent manner. In particular, purine metabolic pathways were differentially changed in the two cell lines. The expression of ribonucleoside-diphosphate reductase subunit M2 (RRM2) was increased in ATM-wild type cells at both mRNA and protein levels, but no changes were detected in ATM-mutated cells. Increased expression of p53 was observed 30min after irradiation of the ATM-wild type cells. These results suggest that RRM2 is a downstream target of the ATM-p53 pathway that mediates radiation-induced DNA repair. We demonstrated that the integrated bioinformatics approach facilitated pathway analysis, hypothesis generation and target gene/protein identification.
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.