ArticleBioinformatics (Oxford, England)2008
Gain and loss of phosphorylation sites in human cancer.
Article in Bioinformatics (Oxford, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- Computational analysis of the structural and functional impact of the deleterious nsSNPs in the humanBiochemistry and biophysics reports · 2026Article
- GnomAD Missense Variants of Uncertain Significance: Implications for p53 Stability and Phosphorylation.International journal of molecular sciences · 2025Article
- Post-translational modifications of immune checkpoints: unlocking new potentials in cancer immunotherapy.Experimental hematology & oncology · 2025Review
- A Novel Missense Variant ofHuman mutation · 2025Article
- Post-translational modifications and their implications in cancer.Frontiers in oncology · 2023Review
- Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR-Mediated Base Editors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Development and Validation of AMBER-FB15-Compatible Force Field Parameters for Phosphorylated Amino Acids.The journal of physical chemistry. B · 2021Article
- Proteo-transcriptomics meta-analysis identifies SUMO2 as a promising target in glioblastoma multiforme therapeutics.Cancer cell international · 2021Article
- Src acts as the target of matrine to inhibit the proliferation of cancer cells by regulating phosphorylation signaling pathways.Cell death & disease · 2021Article
- A global map of associations between types of protein posttranslational modifications and human genetic diseases.iScience · 2021Article
- ActiveDriverDB: Interpreting Genetic Variation in Human and Cancer Genomes Using Post-translational Modification Sites and Signaling Networks (2021 Update).Frontiers in cell and developmental biology · 2021Article
- PhosphoEffect: Prioritizing Variants On or Adjacent to Phosphorylation Sites through Their Effect on Kinase Recognition Motifs.iScience · 2020Article
- Article
- Label-free diagnostics and cancer surgery Raman spectra guidance for the human colon at different excitation wavelengths.RSC advances · 2019Article
- Article
- Pathogenicity and functional impact of non-frameshifting insertion/deletion variation in the human genome.PLoS computational biology · 2019Article
- A Methodological Assessment and Characterization of Genetically-Driven Variation in Three Human Phosphoproteomes.Scientific reports · 2018Article
- Intrinsic Disorder and Posttranslational Modifications: The Darker Side of the Biological Dark Matter.Frontiers in genetics · 2018Review
- Proteogenomic analysis prioritises functional single nucleotide variants in cancer samples.Oncotarget · 2017Article
- Quantitative Phosphoproteomic Analysis Reveals Key Mechanisms of Cellular Proliferation in Liver Cancer Cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
motivationCoding-region mutations in human genes are responsible for a diverse spectrum of diseases and phenotypes. Among lesions that have been studied extensively, there are insights into several of the biochemical functions disrupted by disease-causing mutations. Currently, there are more than 60 000 coding-region mutations associated with inherited disease catalogued in the Human Gene Mutation Database (HGMD, August 2007) and more than 70 000 polymorphic amino acid substitutions recorded in dbSNP (dbSNP, build 127). Understanding the mechanism and contribution these variants make to a clinical phenotype is a formidable problem.
resultsIn this study, we investigate the role of phosphorylation in somatic cancer mutations and inherited diseases. Somatic cancer mutation datasets were shown to have a significant enrichment for mutations that cause gain or loss of phosphorylation when compared to our control datasets (putatively neutral nsSNPs and random amino acid substitutions). Of the somatic cancer mutations, those in kinase genes represent the most enriched set of mutations that disrupt phosphorylation sites, suggesting phosphorylation target site mutation is an active cause of phosphorylation deregulation. Overall, this evidence suggests both gain and loss of a phosphorylation site in a target protein may be important features for predicting cancer-causing mutations and may represent a molecular cause of disease for a number of inherited and somatic mutations.
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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.