APE1 _ APEX1 Antibody
- Known as:
- APE1 _ APEX1 Antibody
- Catalog number:
- AF1071a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- APE1 _ APEX1 Antibody
Related genes to: APE1 _ APEX1 Antibody
- Gene:
- APEX1 NIH gene
- Name:
- apurinic/apyrimidinic endodeoxyribonuclease 1
- Previous symbol:
- APEX
- Synonyms:
- APE, REF1, HAP1, APX, APEN, REF-1, APE-1
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2016-03-08
Related products to: APE1 _ APEX1 Antibody
Related articles to: APE1 _ APEX1 Antibody
- Human apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APE1) is a multifunctional protein central to DNA repair and redox regulation, yet its dynamic post-translational modifications (PTMs) remain poorly understood. Here, we report a biotin-regulated avidin-based nano-catcher (bMIPAPE1) capable of capturing active APE1 in living cells. By leveraging biotin-saturated avidin assembled onto magnetic nanoparticles and surface-imprinted with polydopamine, we engineered highly specific binding cavities for APE1 that enable retention of labile PTMs. This platform revealed 25 previously unreported PTMs across 18 residues of APE1, encompassing acetylation, phosphorylation, ubiquitination, methylation, S-nitrosylation, palmitoylation, and succinylation, and highlighting several PTM hotspots. Representative modifications include phosphorylation at Y264 and Y269, and acetylation at K63, with several PTMs associated with APE1 nuclear export. In addition to high specificity and intracellular compatibility, bMIPAPE1 attenuated both the DNA repair and redox-related functions of APE1. Our findings demonstrate the utility of artificial nanocomposites as tools for live-cell PTM profiling and functional modulation of target proteins, offering a powerful approach to decode protein regulation in living systems and identify potential therapeutic targets in cancer. - Source: PubMed
Zhang RuilanXie HuaisyuanZhu ChenxuSun YingLi KexuanLi HongweiNiu XiaogangJin ChangwenZhao Meiping - - Source: PubMed
Publication date: 2026/04/03
Anisha J PShynu MRadhika GBeena VUma RLijo JAsaf V N MuhasinGleeja V L - G-quadruplexes (G4s) are non-canonical DNA secondary structures enriched at promoters, yet their regulatory role in transcription remains elusive. While G4-ligand-based studies suggest transcriptional repression, their prevalence at oncogene promoters and correlation with high expression suggest a positive regulatory role. Here, we provide direct genetic evidence that promoter G4s function as positive activators of gene expression through a novel mechanism. By selectively mutating endogenous promoter G4 motifs, we demonstrate that G4 loss significantly impairs oncogene expression. Using the endogenous CXCL1 promoter G4 as an example, we revealed that loss of a single promoter G4 motif led to a marked down-regulation of CXCL1 expression as well as inhibition of cellular functions such as cell migration and invasion. Mechanistically, we identified apurinic/apyrimidinic endonuclease (APE1), a multifunctional DNA repair and redox factor, as a G4-binding protein which was recruited to promoters via its unique N-terminus. Subsequently, the redox activity of APE1 enhances transcription factor binding at G4-containing promoters, driving a pro-metastatic gene expression program. Disruption of the G4-APE1 interaction, either genetically or pharmacologically, suppresses gene expression and impairs tumor cell malignant traits. Our findings establish a direct genetic link and mechanistic basis for promoter G4s as crucial drivers of oncogene expression and tumor progression. - Source: PubMed
Chen YinglingMohapatra BhopalPramanik SuraviTarpley MasonKalluchi AchyuthRay SutapaHewitt KyleRowley M JordanBand VimlaBhakat Kishor K - TFEB (transcription factor EB) regulates the expression of autophagy and lysosomal genes, is activated by various cellular stresses, and plays a key role in maintaining cellular homeostasis. Recent work demonstrates that TFEB is activated during lysosomal damage through two distinct mechanisms: ATG conjugation-dependent and -independent. TFEB activation proceeds sequentially through two modes. In the early ATG conjugation-independent mode (Mode I), APEX1 interacts with TFEB in the nucleus, maintaining its transcriptional activity and protein stability. In the later ATG conjugation-dependent mode (Mode II), CCT7 and TRIP6 translocate to lysosomes and interact with TFEB, modulating its phosphorylation and nuclear localization. Moreover, TFEB regulation induced by other cellular stresses-such as oxidative stress, proteasome inhibition, mitochondrial damage, and DNA damage-also involves either Mode I or Mode II. Our findings provide new insights into a unified understanding of TFEB regulation under diverse cellular stress conditions. - Source: PubMed
Publication date: 2026/03/30
Shima TakayukiNakamura Shuhei - The present study investigated the effects of seafood-related dietary cadmium (Cd) levels on the survival, growth, biochemical constituents, digestive and metabolic enzyme activities, and antioxidant status of zebrafish (Danio rerio) over a 45-day period. Zebrafish were fed Artemia flakes (AF) containing 0 mg kg Cd (control) and four environmentally relevant concentrations representative of seafood contamination: 0.3 mg kg (permissible limit), 1 mg kg (minimum), 3 mg kg (median), and 5 mg kg (maximum). The results revealed significant Cd-induced toxicity across multiple biological parameters. Survival rate, growth performance, food index, biochemical constituents, and digestive enzyme activities exhibited marked alterations in zebrafish exposed to varying dietary Cd levels compared with the control. Antioxidant and metabolic enzyme activities showed dose-dependent responses, with stimulation at lower Cd levels and inhibition at higher concentrations. Elevated lipid peroxidation observed at higher Cd doses indicated oxidative stress, suggesting that reduced antioxidant capacity leads to increased free radical generation and lipid membrane damage. Gene expression analysis further showed upregulation of sod1, cat, nqo1, and ogg1 at low Cd levels, followed by sharp suppression of these genes. Dose dependent dysregulation was recorded in mbpa and gfap genes, whereas, strong downregulation of gsta1 and apex1 was observed in zebrafish at higher Cd exposure indicating neurotoxicity and impaired genomic repair under severe stress. Overall, the findings demonstrate that chronic exposure to seafood-derived dietary Cd can adversely affect the biological and physiological responses of zebrafish. This implies potential health risks for seafood consumers and highlights the need for regular monitoring of heavy metal contamination in seafood to ensure consumer safety. - Source: PubMed
Publication date: 2026/03/21
Yogeshwaran ArumugamSubashchandrabose MadhavanAnandhan KrishnanThangal Said HamidMuralisankar Thirunavukkarasu