ArticleMolecular biology reports2008
Identification of TCP10L as primate-specific gene derived via segmental duplication and homodimerization of TCP10L through the leucine zipper motif.
Article in Molecular biology reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- TCP10L negatively regulates alpha-fetoprotein expression in hepatocellular carcinoma.BMB reports · 2020Article
- TCP10L synergizes with MAD1 in transcriptional suppression and cell cycle arrest through mutual interaction.BMB reports · 2016Article
- Genome-Wide Association and Exome Sequencing Study of Language Disorder in an Isolated Population.Pediatrics · 2016Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TCP10L, a transcriptional repression factor gene that was localized on human chromosome 21q22.11, was identified to be derived through segmental duplication since the divergence of primates and rodents. It was elucidated that TCP10L gene was a primate-specific gene in this study. Subsequently it was demonstrated that the putative leucine zipper motif mediated the homodimerization of TCP10L. Using in vitro and in vivo methodologies, it was shown that either deletion or point mutation of the leucine zipper motif was sufficient to abolish TCP10L homodimerization. In Hela cells, both the exogenous wild type TCP10L and endogenous TCP10L were detected on nuclei with immunofluorescence assay. However, the leucine zipper motif mutants of TCP10L could also be detected on nuclei. The results suggested that the leucine zipper motif enabled TCP10L to homodimerize, but was not essential for the TCP10L nuclear localization.
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