ArticleNature communications2023
The HAPSTR2 retrogene buffers stress signaling and resilience in mammals.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Chemogenetic ubiquitin E1 inhibitor TAK-243 CRISPR screen uncovers HAPSTR1/HUWE1 axis in chromatin proteostasis and cell cycle control.Science advances · 2026Article
- Novel insights into retrogene evolution and cold adaptation in the alpine plant Crucihimalaya himalaica (Brassicaceae).BMC biology · 2026Article
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- Comprehensive computational insights into Plasmodium retrocopies reveals potential roles in virulence-associated functions.Genetica · 2026Article
- Tight regulation of a nuclear HAPSTR1-HUWE1 pathway essential for mammalian life.Life science alliance · 2024Article
- Interchromosomal Colocalization with Parental Genes Is Linked to the Function and Evolution of Mammalian Retrocopies.Molecular biology and evolution · 2023Article
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Authors and funding
8 authors.
Funding
Abstract
We recently identified HAPSTR1 (C16orf72) as a key component in a novel pathway which regulates the cellular response to molecular stressors, such as DNA damage, nutrient scarcity, and protein misfolding. Here, we identify a functional paralog to HAPSTR1: HAPSTR2. HAPSTR2 formed early in mammalian evolution, via genomic integration of a reverse transcribed HAPSTR1 transcript, and has since been preserved under purifying selection. HAPSTR2, expressed primarily in neural and germline tissues and a subset of cancers, retains established biochemical features of HAPSTR1 to achieve two functions. In normal physiology, HAPSTR2 directly interacts with HAPSTR1, markedly augmenting HAPSTR1 protein stability in a manner independent from HAPSTR1's canonical E3 ligase, HUWE1. Alternatively, in the context of HAPSTR1 loss, HAPSTR2 expression is sufficient to buffer stress signaling and resilience. Thus, we discover a mammalian retrogene which safeguards fitness.
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