Ask about this productRelated genes to: A1CF antibody
- Gene:
- A1CF NIH gene
- Name:
- APOBEC1 complementation factor
- Previous symbol:
- -
- Synonyms:
- ACF, ASP, ACF64, ACF65, APOBEC1CF
- Chromosome:
- 10q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2007-11-23
- Date modifiied:
- 2016-10-05
Related products to: A1CF antibody
Related articles to: A1CF antibody
- Teratozoospermia is an abnormal sperm morphology that is a common cause of male infertility. Epigenetic factors have been implicated in the regulation of gene expression in teratozoospermia, but the specific mechanisms are not fully understood. This study aimed to identify differentially expressed genes (DEGs) between teratozoospermia and normozoospermia samples, and to investigate the role of epigenetic regulatory factors in the observed gene expression changes. The study integrated data from three publicly available datasets in the GSE6969 superseries. The DEGs were compared to a list of known human epigenetic-related genes obtained from the EpiFactors database. The protein-protein interaction (PPI) network and hub gene identifications for Epi-DEGs and the RNA-protein interaction (RPI) network to obtained the RBPs interacting with Epi-DEGs were constructed. siRNA design for the candidate mRNA was performed using various bioinformatics tools. As a result, the obtained 1,292 DEGs were compared to a list of 796 known human epigenetic factors, revealing 63 Epi-DEGs. The PPI network of Epi-DEGs identified top 10 hub genes including , , , , , , , , and . The RPI network analysis revealed , and as key RNA-binding protein regulators epigenetic modifiers. Based on these findings, the study designed the sequence GCAACAAGAGAAGAA GCAATT as an optimal siRNA candidate targeting the master regulator IGF2BP2, which exhibited the most significant change in expression among the RNA-binding proteins (RBPs). This integrative analysis sheds light on the epigenetic mechanisms underlying teratozoospermia and highlights the potential of RBPs as diagnostic biomarkers and therapeutic targets for further investigation. - Source: PubMed
Mousavi Seyedeh ZahraMohammad-Soltani BahramHadizadeh MortezaRokhsattalab ZeynabTotonchi Mehdi - Lupus nephritis (LN) is the most common complication of systemic lupus erythematosus. CircRNA MTND5 (circMTND5) contributes to the pathogenesis of LN by sponging miR6812. However, it remains unclear what role RNA binding protein to circMTND5 might play. We investigated whether circMTND5 interacts with RNA binding proteins (RBP) in the progression of LN, and to clarify the mechanisms. - Source: PubMed
Publication date: 2025/08/23
Ma CongLuan JunjunJiao CongcongHao XiangnanFu JingqiKopp Jeffrey BPi JingboZhou Hua - Adenomatous polyposis confers an increased risk of developing colorectal cancer. and are the major genes investigated in patients suspected of having polyposis. In addition to and genes, other genes, such as , and , have recently been associated with polyposis phenotypes, conferring heterogeneity in terms of the clinical, etiological and heritable aspects of patients with polyposis. - Source: PubMed
Dos Santos WellingtonPereira Ariane SLaureano Thaisde Andrade Edilene SReis Monise TGarcia Felipe AoCampacci NataliaMelendez Matias EReis Rui MGalvão Henrique de CrPalmero Edenir I - Type 2 diabetes (T2D) is a devastating chronic disease marked by pancreatic β cell dysfunction and insulin resistance, whose pathophysiology remains poorly understood. HNF1A, which encodes transcription factor hepatocyte nuclear factor-1 alpha, is the most commonly mutated gene in Mendelian diabetes. HNF1A also carries loss- or gain-of-function coding variants that respectively predispose to or protect against polygenic T2D. The mechanisms underlying HNF1A-deficient diabetes, however, are still unclear. We now demonstrate that diabetes arises from β cell-autonomous defects and identify direct β cell genomic targets of HNF1A. This uncovered a regulatory axis where HNF1A controls transcription of A1CF, which orchestrates an RNA splicing program encompassing genes that regulate β cell function. This HNF1A-A1CF transcription-splicing axis is suppressed in β cells from T2D individuals, while genetic variants reducing pancreatic islet A1CF are associated with increased glycemia and T2D susceptibility. Our findings, therefore, identify a linear hierarchy that coordinates β cell-specific transcription and splicing programs and link this pathway to T2D pathogenesis. - Source: PubMed
Publication date: 2025/08/06
Bernardo EdgarDe Vas Matías GonzaloBalboa DiegoCuenca-Ardura MirabaiBonàs-Guarch SílviaPlanas-Fèlix MercèMollandin FannyTorrens-Dinarès MiquelMaestro Miguel AngelGarcía-Hurtado JavierMoratinos SoniaRavassard PhilippeDou HaiqiangHeyn Holgervan Oudenaarden AlexanderGroen Nathaliede Koning EelcoConrad ChristianEils RolandVernia SantiagoRorsman PatrikFerrer Jorge - Sepsis-associated liver injury (SLI) is a common complication of sepsis, for which effective therapeutic strategies are lacking. DNA methylation and hydroxymethylation play crucial roles in the regulation of gene expression. This study investigated the effects of metformin on the DNA methylation landscape in a rat model of cecal ligation and puncture (CLP)-induced SLI. Reduced representation bisulfite sequencing (RRBS) and oxidative RRBS (ox-RRBS) were used to assess global DNA methylation and hydroxymethylation patterns in the liver tissues. The results showed that CLP-induced SLI was associated with global DNA hypomethylation and hyperhydroxymethylation, which were partially reversed by metformin treatment. The expression levels of DNA methyltransferases and ten-eleven translocation 2 (TET2) were elevated in the CLP group and were modulated by metformin. Functional enrichment analysis of differentially methylated and hydroxymethylated genes revealed their involvement in oxidative phosphorylation and metabolic pathways. Furthermore, integration of DNA methylation, hydroxymethylation, and transcriptome data identified two genes, A1cf and Atxn7l1, that exhibited increased methylation and decreased expression in CLP, which were reversed by metformin treatment. These findings provide novel insights into the epigenetic mechanisms underlying SLI and suggest that metformin exerts hepatoprotective effects by modulating DNA methylation and hydroxymethylation. - Source: PubMed
Publication date: 2025/05/07
Liu FengyuTong RanSong HengGong LinmeiDing XianfeiLiu HuanLi HongyiLiu LimingWang YuzeZhang RuipengSun Tongwen