ArticlePLoS genetics2007
Repeated recruitment of LTR retrotransposons as promoters by the anti-apoptotic locus NAIP during mammalian evolution.
Article in PLoS genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 125 citations in OpenAlex.
- Host-transposon mutualism supports regeneration in planarians.Developmental cell · 2026Article
- BAT: an integrated pipeline for gene tree construction, annotation, and functional inference.bioRxiv : the preprint server for biology · 2026Article
- Expression spectrum of TE-driven transcripts in human adult tissues.Genome biology · 2026Article
- Transposable elements drive evolution and perturb gene expression in Brassica rapa and B. oleracea.The Plant journal : for cell and molecular biology · 2025Article
- Gene expression in soft-shell clam (Mya arenaria) transmissible cancer reveals survival mechanisms during host infection and seawater transfer.PLoS genetics · 2025Article
- Adaptive expansion of ERVK solo-LTRs is associated with Passeriformes speciation events.Nature communications · 2024Article
- Correlation of Myeloid-Derived Suppressor Cell Expansion with Upregulated Transposable Elements in Severe COVID-19 Unveiled in Single-Cell RNA Sequencing Reanalysis.Biomedicines · 2024Article
- Endogenous retroviral solo-LTRs in human genome.Frontiers in genetics · 2024Review
- Progressive Exaptation of Endogenous Retroviruses in Placental Evolution in Cattle.Biomolecules · 2023Review
- Human and mouse NAIP/NLRC4 inflammasome responses to bacterial infection.Current opinion in microbiology · 2023Review
- Salmonella enterica Serovar Typhimurium Induces NAIP/NLRC4- and NLRP3/ASC-Independent, Caspase-4-Dependent Inflammasome Activation in Human Intestinal Epithelial Cells.Infection and immunity · 2022Article
- Zebrafish transposable elements show extensive diversification in age, genomic distribution, and developmental expression.Genome research · 2022Article
- Human NAIP/NLRC4 and NLRP3 inflammasomes detect Salmonella type III secretion system activities to restrict intracellular bacterial replication.PLoS pathogens · 2022Article
- Endogenous retroviruses in the origins and treatment of cancer.Genome biology · 2021Review
- Phylogenomics of the Maverick Virus-Like Mobile Genetic Elements of Vertebrates.Molecular biology and evolution · 2021Article
- Tissue-specific usage of transposable element-derived promoters in mouse development.Genome biology · 2020Article
- Transposable elements teach T cells new tricks.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Short interspersed nuclear element (SINE)-mediated post-transcriptional effects on human and mouse gene expression: SINE-UP for active duty.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Viewing Legionella pneumophila Pathogenesis through an Immunological Lens.Journal of molecular biology · 2019Review
- Human transposons are an abundant supply of transcription factor binding sites and promoter activities in breast cancer cell lines.Mobile DNA · 2019Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal apoptosis inhibitory protein (NAIP, also known as BIRC1) is a member of the conserved inhibitor of apoptosis protein (IAP) family. Lineage-specific rearrangements and expansions of this locus have yielded different copy numbers among primates and rodents, with human retaining a single functional copy and mouse possessing several copies, depending on the strain. Roles for this gene in disease have been documented, but little is known about transcriptional regulation of NAIP. We show here that NAIP has multiple promoters sharing no similarity between human and rodents. Moreover, we demonstrate that multiple, domesticated long terminal repeats (LTRs) of endogenous retroviral elements provide NAIP promoter function in human, mouse, and rat. In human, an LTR serves as a tissue-specific promoter, active primarily in testis. However, in rodents, our evidence indicates that an ancestral LTR common to all rodent genes is the major, constitutive promoter for these genes, and that a second LTR found in two of the mouse genes is a minor promoter. Thus, independently acquired LTRs have assumed regulatory roles for orthologous genes, a remarkable evolutionary scenario. We also demonstrate that 5' flanking regions of IAP family genes as a group, in both human and mouse are enriched for LTR insertions compared to average genes. We propose several potential explanations for these findings, including a hypothesis that recruitment of LTRs near NAIP or other IAP genes may represent a host-cell adaptation to modulate apoptotic responses.
Indexed as
Identifiers
What OpenQuestion holds
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.