Ask about this productRelated genes to: ApoBEC1 Blocking Peptide
- Gene:
- APOBEC1 NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic subunit 1
- Previous symbol:
- -
- Synonyms:
- BEDP, CDAR1, APOBEC-1, HEPR
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-26
- Date modifiied:
- 2016-10-05
Related products to: ApoBEC1 Blocking Peptide
Related articles to: ApoBEC1 Blocking Peptide
- Spontaneous ovarian hyperstimulation syndrome (OHSS) is closely associated with follicle stimulating hormone receptor (FSHR) functional mutations. We observed that estrildid finches naturally carry the gain-of-function FSHR p.Thr449Ala mutation found in humans, yet do not develop OHSS, thereby providing a novel and system to study aspects of OHSS prevention. Cross-species single-cell analysis revealed that macrophages, the most abundant immune cells in ovaries, play a pivotal role in OHSS progression. Macrophage depletion exacerbates the manifestations of OHSS in both birds and rats. Pharmacological activation of the G protein-coupled receptor 183 (GPR183) in ovarian macrophages, significantly alleviates OHSS symptoms. Mechanistically, GPR183 activation in macrophages maintains ovarian immune homeostasis by downregulating inflammatory factors (Interleukin 1 alpha: IL1A, Interleukin 6: IL6, Interleukin 1 beta: IL1B) and upregulating immune regulators responsive to external stimuli (sphingomyelin phosphodiesterase acid like 3A: Smpdl3a, Macrophage-expressed gene 1: Mpeg1, Epithelial stromal interaction 1: Epsti1, Unc-93 homolog B1: Unc93b1, Apolipoprotein B mRNA editing enzyme catalytic subunit 1: Apobec1). It markedly altered CD44 molecule (CD44)/Syndecan-4 (SDC4) -mediated intercellular communication between macrophages and endothelial/stromal cells, thereby modulating the ovarian microenvironment. This study identifies ovarian macrophages as a key therapeutic target for OHSS and proposes GPR183 as a novel receptor target for precision macrophage-based interventions. - Source: PubMed
Publication date: 2026/05/05
Yan XiaofeiHuang YongjieYang JiabaoMa SuLiu SongsongHuang XuanBrosius JuergenZheng HuapingYao BingChen LiLai ShanshanDeng Cheng - Aberrant expression of the cytidine DNA deaminase AID in enterocytes within inflamed mucosa in ulcerative colitis (UC) patients has been proposed to be involved in progression of UC to colitis-associated colorectal cancer (CA-CRC). Here, we followed the expression of AID and other nuclear cytidine DNA deaminases of the APOBEC family through several stages of progression of UC in a CA-CRC case (UC progressor) and in a cohort of UC progressors and non-progressors. In inflamed and high-grade dysplastic mucosa, and mRNAs, but not -family enzyme mRNAs, were overexpressed compared to non-inflamed tissue. Immunohistochemical staining did not show expression of AID or APOBEC3 enzymes in the enterocytes, neither in specimens from the CA-CRC case nor in biopsies from the progressor and non-progressor cohort. APOBEC1 was highly expressed in the enterocytes throughout the colorectum from the CA-CRC case and in most biopsies examined from the progressor and non-progressor cohort. The expression was not correlated with the histology of the mucosa or the progression status of the patients. In the CA-CRC case, we identified AID- and APOBEC3-associated mutation signatures in inflamed, high-grade dysplasia and cancer genomes. In conclusion, our findings suggest that AID or other nuclear APOBECs are unlikely to drive the progression of UC to CA-CRC late during course of UC. However, we cannot exclude the possibility that bursts of AID and nuclear APOBEC3 activity may contribute to formation of genome instability in early phases of disease development. - Source: PubMed
Publication date: 2026/04/13
Alsøe LeneBrackmann Stephan AndreasLiu YanWennerström Anna BeritEsbensen Qin YingKalyanasundaram SumanaLefol YohanDomanska DianaAndersen Solveig NorheimNilsen Hilde Loge - STAMP (Surveying Targets by APOBEC-Mediated Profiling) employed the fusion protein between an RBP and the C-to-U editing enzyme APOBEC1 to mark and determine RBP's target transcripts. It exhibited wonderful performance in mammals, however, it was confirmed not working in flies and unclear its generality. In this study, APOBEC1 in STAMP was replaced with an APOBEC1-H122L/D124N mutant (APO1m), so that the method HyperSTAMP was established here in flies. HyperSTAMP method effectively and semi-quantitatively uncovered the targets of both Hrp48 (Heterogeneous nuclear ribonucleoprotein 48) and Thor in S2 cells with good signal to noise ratio, reproducibility, and consistency with other methods. It also captured RBP-binding positions on mRNAs through editing clusters on target RNAs. This study filled in the gap of lacking C-to-U editing enzyme in insects and provided a good tool for the experiments of double labeling RNA when exploring multiple RBPs concurrently. - Source: PubMed
Publication date: 2026/03/14
Li ChongJia YunxiaoYe TongZheng LitingSong WeiPiao WeilanQi ChanghaiJin Hua - APOBEC1-based cytosine base editors such as BE4max enable base conversion, but many alternative deaminases show low activity and cytotoxicity, especially when miniaturized for delivery. SsdA, a DNA deaminase toxin from Pseudomonas syringae that is two-thirds the size of APOBEC1, is attractive for compact base editors but, in native form, shows low C-to-T editing efficiency and high cytotoxicity. Guided by an AlphaFold- and CASTpFold-based alanine scan, we identified K31 as a gatekeeping residue whose substitution enlarges the modeled DNA binding pocket. Site-saturation mutagenesis at K31 produced variants with ten-fold higher activity but increased indel formation. To further enhance activity while reducing indels and cytotoxicity, we developed Trinity-Screen, an Escherichia coli (E. coli)-based three-in-one directed evolution platform that selects for high activity and reduced double-strand break-associated indels. Trinity-Screen revealed four additional DNA-binding positions; combinatorial mutagenesis at these sites generated four- and five-site SsdA variants that retained high activity yet showed lower indel rates and rescued bacterial viability. To standardize comparisons, we defined the Base Editor Performance Index (BEPI), which integrates C-to-T conversion and indel frequency. Optimized SsdA variants achieved up to 31-fold improvement relative to wild type, outperforming BE4max at multiple endogenous targets and displaying ten-fold lower cytotoxicity in E. coli. - Source: PubMed
Publication date: 2026/02/03
Gang Son RyeoKim GoeunLee Jungjoon K - Progranulin (PGRN) is a neurotrophic and anti-inflammatory factor produced mainly by neurons and microglia in the central nervous system. Progranulin haploinsufficiency causes frontotemporal dementia (FTD). It is unclear to what extent neuronal versus microglial PGRN deficiency contributes to FTD pathology. In this study, we restored progranulin in neurons in progranulin knockout mice using Nestin-driven expression of mouse Grn transgene in a knockout background (NesGrn KOBG). They were compared with full PGRN KO mice and floxed control mice that carry a loxP flanked STOP codon in front of mGrn transgene (Grn-flfl). The expected neuron-only PGRN rescue was confirmed at RNA and protein level in brain tissue and primary cells, and single nucleus RNA sequencing. Despite neuronal PGRN-restoration, there was no difference in microgliosis, astrogliosis, and microglia phenotypes as assessed by histology, microglia morphometry and bulk RNAseq showing strong upregulation of microglia-associated genes equally in both KO lines. However, a microglial subpopulation with a phagocyte signature expressing Gpnmb, Lgals3, Atp6v0d2 and Apobec1 occurred only in PGRN KO brain, and accordingly, the loss of synapses and dendritic spines, which is caused by excessive synaptic pruning in PGRN KO mice, was partially attenuated in NesGrn KOBG mice. Lipidomic studies showed that phosphatidylserine eat-me-signals were increased in PGRN KO but not in NesGrn KOBG brain. Furthermore, some neuronal genes involved in axonal structure and dynamics were co-restored with progranulin in NesGrn KOBG mice. However, the modest improvement of neuronal health was not associated with an improvement of FTD-like behavior including hyperactivity, compulsive licking and impaired avoidance learning and memory. The results suggest that (still) viable neurons do not provide (sufficient) progranulin to prevent microgliosis but may shape the phenotype by presenting or hiding eat-me signals. Nonetheless, neuron-only-progranulin restoration may be insufficient to halt the progression of FTD. - Source: PubMed
Publication date: 2026/01/10
Weyer Marc-PhilippHahnefeld LisaFranck LuisaAngioni CarloKlein MatthiasGeisslinger GerdSchäfer Michael K ETegeder Irmgard