ArticleNucleic acids research2009
Creation of the two isoforms of rodent NKG2D was driven by a B1 retrotransposon insertion.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- ACLY promotes NK cell effector function by regulating glycolysis and histone acetylation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A promising natural killer cell-based model and a nomogram for the prognostic prediction of clear-cell renal cell carcinoma.European journal of medical research · 2024Article
- Expression dynamics and relations with nearby genes of rat transposable elements across 11 organs, 4 developmental stages and both sexes.BMC genomics · 2017Article
- The impact of transposable elements on mammalian development.Development (Cambridge, England) · 2016Review
- Transposable elements and viruses as factors in adaptation and evolution: an expansion and strengthening of the TE-Thrust hypothesis.Ecology and evolution · 2012Article
- Retrotransposons as a major source of epigenetic variations in the mammalian genome.Epigenetics · 2012Article
- Role of runt-related transcription factor 3 (RUNX3) in transcription regulation of natural cytotoxicity receptor 1 (NCR1/NKp46), an activating natural killer (NK) cell receptor.The Journal of biological chemistry · 2012Article
- A novel protein isoform of the multicopy human NAIP gene derives from intragenic Alu SINE promoters.PloS one · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mouse gene for the natural killer (NK) cell-activating receptor Nkg2d produces two protein isoforms, NKG2D-S and NKG2D-L, which differ by 13 amino acids at the N-terminus and have different signalling capabilities. These two isoforms are produced through differential splicing, but their regulation has not been investigated. In this study, we show that rat Nkg2d has the same splicing pattern as that of the mouse, and we mapped transcriptional start sites in both species. We found that the splice forms arise from alternative promoters and that the NKG2D-L promoter is derived from a rodent B1 retrotransposon that inserted before mouse-rat divergence. This B1 insertion is associated with loss of a nearby splice acceptor site that subsequently allowed creation of the short NKG2D isoform found in mouse but not human. Transient reporter assays indicate that the B1 element is a strong promoter with no inherent lymphoid tissue-specificity. We have also identified different binding sites for the ETS family member GABP within both the mouse and rat B1 elements that are necessary for high-promoter activity and for full Nkg2d-L expression. These findings demonstrate that a retroelement insertion has led to gene-regulatory change and functional diversification of rodent NKG2D.
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