ArticleNucleic acids research2004
Bioinformatical assay of human gene morbidity.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- A Systematic Review of the Human Accelerated Regions in Schizophrenia and Related Disorders: Where the Evolutionary and Neurodevelopmental Hypotheses Converge.International journal of molecular sciences · 2023Pooled it
- Vitamin K preserves gamma-glutamyl carboxylase activity against carbamylations in uremia: Implications for vascular calcification and adjunct therapies.Acta physiologica (Oxford, England) · 2025Article
- Low expression of PEBP1P2 promotes metastasis of clear cell renal cell carcinoma by post-transcriptional regulation of PEBP1 and KLF13 mRNA.Experimental hematology & oncology · 2022Article
- Negative selection on human genes underlying inborn errors depends on disease outcome and both the mode and mechanism of inheritance.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Properties of human disease genes and the role of genes linked to Mendelian disorders in complex disease aetiology.Human molecular genetics · 2017Article
- The essential and downstream common proteins of amyotrophic lateral sclerosis: A protein-protein interaction network analysis.PloS one · 2017Article
- The role of mutation rate variation and genetic diversity in the architecture of human disease.PloS one · 2014Article
- The relationship between gene isoform multiplicity, number of exons and protein divergence.PloS one · 2013Article
- A new essential protein discovery method based on the integration of protein-protein interaction and gene expression data.BMC systems biology · 2012Article
- Defining the role of essential genes in human disease.PloS one · 2011Article
- The interplay between evolution, regulation and tissue specificity in the Human Hereditary Diseasome.BMC genomics · 2010Article
- Advances in translational bioinformatics: computational approaches for the hunting of disease genes.Briefings in bioinformatics · 2010Article
- Correlation of microsynteny conservation and disease gene distribution in mammalian genomes.BMC genomics · 2009Article
- Similarly strong purifying selection acts on human disease genes of all evolutionary ages.Genome biology and evolution · 2009Article
- Quantifying dominance and deleterious effect on human disease genes.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- An ancient evolutionary origin of genes associated with human genetic diseases.Molecular biology and evolution · 2008Article
- Natural selection on genes that underlie human disease susceptibility.Current biology : CB · 2008Article
- Natural selection of protein structural and functional properties: a single nucleotide polymorphism perspective.Genome biology · 2008Article
- Role of duplicate genes in robustness against deleterious human mutations.PLoS genetics · 2008Article
- Bioinformatic analysis of human CNS-expressed ion channels as candidates for episodic nervous system disorders.Neurogenetics · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Only a fraction of eukaryotic genes affect the phenotype drastically. We compared 18 parameters in 1273 human morbid genes, known to cause diseases, and in the remaining 16 580 unambiguous human genes. Morbid genes evolve more slowly, have wider phylogenetic distributions, are more similar to essential genes of Drosophila melanogaster, code for longer proteins containing more alanine and glycine and less histidine, lysine and methionine, possess larger numbers of longer introns with more accurate splicing signals and have higher and broader expressions. These differences make it possible to classify as non-morbid 34% of human genes with unknown morbidity, when only 5% of known morbid genes are incorrectly classified as non-morbid. This classification can help to identify disease-causing genes among multiple candidates.
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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.