ArticleChromosoma2012
Putative CENP-B paralogues are not present at mammalian centromeres.
Article in Chromosoma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Single-cell analysis of TIGD genes in hepatocellular carcinoma: Prognostic value and functional characterization.Translational oncology · 2026Article
- Centromeres drive and take a break.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Review
- Genomic instability genes in lung and colon adenocarcinoma indicate organ specificity of transcriptomic impact on Copy Number Alterations.Scientific reports · 2022Article
- The genetics and epigenetics of satellite centromeres.Genome research · 2022Article
- Phylogenetic analysis of theMobile DNA · 2020Article
- Evolutionary Turnover of Kinetochore Proteins: A Ship of Theseus?Trends in cell biology · 2016Review
- Review
- DNA Sequence-Specific Binding of CENP-B Enhances the Fidelity of Human Centromere Function.Developmental cell · 2015Article
- Pogo-like transposases have been repeatedly domesticated into CENP-B-related proteins.Genome biology and evolution · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although centromere protein B (CENP-B) is a highly conserved mammalian centromere protein, its function remains unknown. The presence of the protein is required to form artificial satellite DNA-based centromeres de novo, yet cenpb knockout mice are viable for multiple generations with no mitotic or meiotic defects, and the protein is not present at fully functional neocentromeres. Previous studies have suggested that the presence of functionally redundant paralogues of CENP-B may explain the lack of a phenotype in knockout mice, and the related Tigger-derived (TIGD) family of proteins has been implicated as the most likely candidate for such paralogues. Here, we describe an investigation of the centromere-binding properties of the three TIGD proteins most highly related to CENP-B through phylogenetic analysis through EGFP fusion studies and immunocytochemistry. Although two of the three proteins bound to human centromeres with low affinity when overexpressed as fusion proteins, the strongest candidate, TIGD3, demonstrated no native centromeric binding when using raised antibodies, either in human cells or in cenpb (-/-) mouse ES cells. We conclude that the existence of functional CENP-B paralogues is highly unlikely and that CENP-B acts alone at the centromere. Based on these data, we suggest a new, meiotic drive model of CENP-B action during centromere repositioning in evolution.
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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.