ArticleProceedings of the National Academy of Sciences of the United States of America2022
Structure and function of an effector domain in antiviral factors and tumor suppressors SAMD9 and SAMD9L.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 45 citations in OpenAlex.
- Functional assessment of inherited myeloid neoplasm-associated SAMD9L germline variants via Monoallelic CRISPR modelling.British journal of haematology · 2026Article
- Structural mechanisms of SAMD9 autoinhibition and pathogenic dysregulation.Science advances · 2026Article
- Genome-wide DNA methylation profiling of triple-negative breast cancer uncovers epigenetic biomarkers of tumor identity and the immune microenvironment.NPJ breast cancer · 2026Article
- From a novel pathogenic SAMD9L variant to cohort-wide insights: Whole-genome sequencing highlights somatic genetic rescue and phenotypic heterogeneity.British journal of haematology · 2026Article
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- Integrative Proteomic and Phosphoproteomic Analysis Reveals Altered Vesicle Transport in Systemic Lupus Erythematosus.Clinical proteomics · 2026Article
- Identification of duck type II interferon-stimulated genes and revelation of duIFI35 inhibition of H5N6 AIV replication by promoting apoptosis.Veterinary research · 2026Article
- Bacterial Schlafen proteins mediate phage defence.Nature microbiology · 2026Article
- Moving Beyond Somatic Alterations: Uncovering the Germline Basis of Myeloid Malignancies.Cancers · 2026Review
- A De Novo Mutation (c.2423A>G) inHuman mutation · 2026Article
- Evolutionary characterization of antiviral SAMD9/9L across kingdoms supports ancient convergence and lineage-specific adaptations.Nature ecology & evolution · 2025Article
- SAMD9L inhibits flavivirus translation independently of its capacity to trigger innate immune response.PLoS pathogens · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Normal Immune Function in a Newborn With Early Identification of aClinical case reports · 2025Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- Article
- Structural and functional studies of rabbit SAMD9 reveal a distinct tRNase module that underlies the antiviral activity.PLoS pathogens · 2025Article
- CryoEM structure of the SLFN14 endoribonuclease reveals insight into RNA binding and cleavage.Nature communications · 2025Article
- Ancient convergence with prokaryote defense and recent adaptations to lentiviruses in primates characterize the ancestral immune factors SAMD9s.bioRxiv : the preprint server for biology · 2025Article
- DnaJ mediates phage sensing by the bacterial NLR-related protein bNACHT25.PLoS biology · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
SAMD9 and SAMD9L (SAMD9/9L) are antiviral factors and tumor suppressors, playing a critical role in innate immune defense against poxviruses and the development of myeloid tumors. SAMD9/9L mutations with a gain-of-function (GoF) in inhibiting cell growth cause multisystem developmental disorders including many pediatric myelodysplastic syndromes. Predicted to be multidomain proteins with an architecture like that of the NOD-like receptors, SAMD9/9L molecular functions and domain structures are largely unknown. Here, we identified a SAMD9/9L effector domain that functions by binding to double-stranded nucleic acids (dsNA) and determined the crystal structure of the domain in complex with DNA. Aided with precise mutations that differentially perturb dsNA binding, we demonstrated that the antiviral and antiproliferative functions of the wild-type and GoF SAMD9/9L variants rely on dsNA binding by the effector domain. Furthermore, we showed that GoF variants inhibit global protein synthesis, reduce translation elongation, and induce proteotoxic stress response, which all require dsNA binding by the effector domain. The identification of the structure and function of a SAMD9/9L effector domain provides a therapeutic target for SAMD9/9L-associated human diseases.
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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.