A1CF
- Known as:
- A1CF
- Catalog number:
- 000852A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- A1CF
Ask about this productRelated genes to: A1CF
- 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
Related articles to: A1CF
- This discovery study investigated the impact of MODY-associated mutations in hepatocyte nuclear factors HNF1A and HNF1B on the cellular proteome, aiming to identify affected pathways and advance understanding of diabetes pathogenesis. Human induced pluripotent stem cells (hiPSCs) carrying the HNF1A frameshift mutation (p.Pro291fsinsC) were differentiated into pancreatic progenitors, and renal proximal tubule epithelial cells (RPTECs) were engineered to overexpress HNF1B with the S148L point mutation. Label-free quantitative proteomics was performed using data-dependent and data-independent acquisition on Orbitrap and timsTOF mass spectrometers. Pathway enrichment was analyzed using Qiagen IPA, Hallmark gene sets, and STRING networks. Comprehensive proteome coverage (over 7000 proteins) revealed consistent downregulation of oxidative phosphorylation, mitochondrial function, and interferon signaling pathways. Both models exhibited suppression of innate immune responses, with overlapping downregulated proteins, including members of the OAS, IFIT, and MX1 families. Using label-free proteomics, we show that MODY-associated mutations in HNF1A and HNF1B suppress mitochondrial function and interferon signaling and are additionally associated with reduced abundance of predicted targets such as A1CF as well as diabetes-related proteins including SCGN, supporting their role in diabetes pathogenesis. - Source: PubMed
Publication date: 2026/08/05
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Publication date: 2026/06/08
Avateffazeli MasoumeRahmati RahemMohammadnia AbdolrezaHajimoradi MaryamNazari ElhamShafaghi Shadi - 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
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