ArticleCell reports2014
Mutation of POLB causes lupus in mice.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 61 citations in OpenAlex.
- Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.International journal of radiation biology · 2026Review
- Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).International journal of molecular medicine · 2026Review
- Review
- DNA polymerase β suppresses somatic indels at CpG dinucleotides in developing cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Preliminary exploration of mRNA, lncRNA, and miRNA expressions in the bovine jejunum unveils novel aspects of Mycobacterium avium subspecies paratuberculosis infections.BMC genomics · 2025Article
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- Molecular characterisation of lupus low disease activity state (LLDAS) and DORIS remission by whole-blood transcriptome-based pathways in a pan-European systemic lupus erythematosus cohort.Annals of the rheumatic diseases · 2024Article
- Mouse models to explore the biological and organismic role of DNA polymerase beta.Environmental and molecular mutagenesis · 2024Review
- Polβ/XRCC1 heterodimerization dictates DNA damage recognition and basal Polβ protein levels without interfering with mouse viability or fertility.DNA repair · 2023Article
- Levels of base excision repair proteins in CD4Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- ATR-mediated DNA damage responses underlie aberrant B cell activity in systemic lupus erythematosus.Science advances · 2022Article
- A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus-like Disease in Mice.ACR open rheumatology · 2022Article
- A novel mechanism for macrophage pyroptosis in rheumatoid arthritis induced by Pol β deficiency.Cell death & disease · 2022Article
- Interlocking activities of DNA polymerase β in the base excision repair pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Autoantibodies against cytoskeletons and lysosomal trafficking discriminate sarcoidosis from healthy controls, tuberculosis and lung cancers.Molecular biomedicine · 2022Article
- ROS and DNA repair in spontaneous versus agonist-induced NETosis: Context matters.Frontiers in immunology · 2022Article
- Defective DNA polymerase beta invoke a cytosolic DNA mediated inflammatory response.Frontiers in immunology · 2022Article
- The hematopoietic compartment is sufficient for lupus development resulting from the POLB-Y265C mutation.PloS one · 2022Article
- DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model.DNA repair · 2021Article
- DNA Damage Response in the Adaptive Arm of the Immune System: Implications for Autoimmunity.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
A replication study of a previous genome-wide association study (GWAS) suggested that a SNP linked to the POLB gene is associated with systemic lupus erythematosus (SLE). This SNP is correlated with decreased expression of Pol β, a key enzyme in the base excision repair (BER) pathway. To determine whether decreased Pol β activity results in SLE, we constructed a mouse model of POLB that encodes an enzyme with slow DNA polymerase activity. We show that mice expressing this hypomorphic POLB allele develop an autoimmune pathology that strongly resembles SLE. Of note, the mutant mice have shorter immunoglobulin heavy-chain junctions and somatic hypermutation is dramatically increased. These results demonstrate that decreased Pol β activity during the generation of immune diversity leads to lupus-like disease in mice, and suggest that decreased expression of Pol β in humans is an underlying cause of SLE.
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.