Ask about this productRelated genes to: Zfp113 antibody
- Gene:
- ZNF3 NIH gene
- Name:
- zinc finger protein 3
- Previous symbol:
- -
- Synonyms:
- A8-51, KOX25, PP838, FLJ20216, HF.12, Zfp113
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-31
- Date modifiied:
- 2016-10-25
Related products to: Zfp113 antibody
Related articles to: Zfp113 antibody
- Rectal carcinoma (RC) represents approximately 30% of all colorectal carcinomas (CRC) and is considered a distinct clinical entity. Vascular invasion (VI) is recognized as an independent predictor of poor outcomes in RC. In this study, we applied bioinformatics methods to identify gene pathways most likely associated with VI in rectal carcinoma. As showed statistically significant negative relations with the VI in RC patients, we further analyzed its top co-dependent genes-DNAL4, EVI2B, PPP1R35, PTGR3, RPL21, SOX4, and ZNF3-for the experimentally proven molecular modulators. We identified a total of 23 compounds from the Comparative Toxicogenomics Database based on previously reported data for all eight target genes. The search was expanded to include additional chemical agents by structure similarity using the PubChem database, which revealed 9661 additional compounds. These were subsequently used for molecular interaction analysis against target proteins co-expressed with, or associated with, in RC with VI. Ultimately, we identified four high-affinity compounds-cyanoginosin LR, doxorubicin, benzo[a]pyrene, and dibenzo(a,e)pyrene-that interacted with all target proteins. These compounds show potential for further assessment of their role in modulating processes related to vascular invasion, which is a strong negative predictor of RC outcomes. - Source: PubMed
Publication date: 2025/06/28
Kožik BojanaČorbo TarikPojskić NarisBožović AnaTodorović LidijaKolaković AnaMandušić VesnaPojskić Lejla - Crosstalk between the post-translational modification processes of ubiquitination and ADP-ribosylation occurs in DNA-damage- and immune-responses, in addition the physical linkage of ADP-ribose and ubiquitin is found during bacterial infection. Here, we study the ubiquitination of ADP-ribose mediated by human Deltex E3 ligases and the subsequent fate of the formed hybrid post-translational modification. We prepare a non-hydrolysable ADPr-Ub probe that we employ in a proteomics approach and identify RNF114 as an interacting protein. Using biophysical and biochemical experiments, we validate that RNF114 preferentially interacts with ubiquitinated ADP-ribose over non-modified ubiquitin. Subsequently, RNF114 can elongate the ubiquitinated ADP-ribose with a K11-linked ubiquitin chain. Using domain deletion analysis, we pinpoint the tandem zinc fingers and ubiquitin interacting motif (ZnF2 + ZnF3+UIM) domains of RNF114 to be crucial for recognising ubiquitinated ADP-ribose. Moreover, these domains are essential for the recruitment of RNF114 to the sites of laser-induced DNA damage. - Source: PubMed
Publication date: 2025/07/09
Kloet Max SChatrin ChatrinMukhopadhyay Rishovvan Tol Bianca D MSmith RebeccaRotman Sarah ATjokrodirijo Rayman T NZhu KangGorelik AndriiMaginn LucyElliott Paul Rvan Veelen Peter AAhel DraganaAhel Ivanvan der Heden van Noort Gerbrand J - Inadequate angiogenesis of endometriotic implants stimulated by the inflammatory microenvironment in the uterine region leads to the development of gynecological diseases, which significantly reduce the fertility and vitality of young women. Angiogenic processes are controlled by factors whose activities are regulated at the gene level by reactive oxygen species (ROS), hypoxia-induced factors (HIFs), and zinc-finger proteins (ZnFs) or posttranscriptionally via non-coding RNAs. The cooperation of these factors is responsible for the manifestation of pathological stimuli in the form of endometriosis of the body of the uterus, ovaries, or peritoneum, from which endometrioid carcinoma can develop. Molecules that can control gene expression by their intercalation to target DNA sequence, such as [Zn(neo)(nif)], could prevent the hyperactivation of pro-angiogenic pathways (decrease HIF-1α, VEGF-A, TGF-β1, COX2, and ANG2/ANG1), reduce the formation of ROS, and reduce the risk of uterine neoplasticity. The NSAID-metal complex [Zn(neo)(nif)] shows an ability to intercalate into ZNF3-7 target DNA sequence at a higher rate, which could explain its effect on genes regulated by this transcription factor. In addition, [Zn(neo)(nif)] affects ROS production and Ca level, possibly pointing to mitochondrial dysfunction as a potential cause for the described apoptosis. - Source: PubMed
Publication date: 2025/03/24
Špaková IvanaSmolko LukášSabolová GabrielaBadovská ZuzanaKalinová KatarínaMadreiter-Sokolowski CorinaGraier Wolfgang FMareková MáriaVašková JankaRabajdová Miroslava - Arsenic is a toxic contaminant that can be found in drinking water. In this study, the development of an efficient electrode as an electrochemical sensor to detect arsenic(v) in drinking water is presented. The surface of ZnO nanorods (NRs) synthesized on a Ni-foam substrate was modified by depositing α-FeO nanoparticles (NPs) to fabricate an electrode for the detection of arsenic(v) contamination in drinking water. This electrode was synthesized through two separate growth steps: a hydrothermal (ZnO NRs) step followed by the dip-coating method (α-FeO NPs). The dip-coating method was repeated multiple times, 2 times (ZNF-2), 3 times (ZNF-3) and 4 times (ZNF-4), in order to achieve a uniform coverage of the ZnO NR surface. The electrodes were characterized using XRD, XPS, SEM and UV-vis spectroscopy. The best efficiency among the α-FeONP-modified nanorod samples was observed for the 3-time dip-coated ZNF-3 sample, which presented a uniform and homogeneous morphology, as observed from the SEM images, accompanied with the highest oxidation current. The electrochemical performance of the sensor electrodes was tested for a wide range of arsenic(v) concentrations from 0 to 50 ppb and was monitored using cyclic voltammetry. The results demonstrated a calibration plot that was linear over a concentration range of 0-50 ppb of arsenic(v), and the regression equation extracted from the calibration curve was found to be = 0.003 - 0.6271 (with = 0.991). The limit of detection (LOD) and limit of quantification (LOQ) were found to be 4.12 ppb and 13.74 ppb, respectively, which are lower than the maximum allowed value recommended by the World Health Organization (WHO) for arsenic in drinking water. This reasonable performance of the ZnO NRs/Ni-foam/α-FeONP nanocomposite electrode can be further enhanced, and the electrode can be utilized for efficient arsenic(v) detection in drinking water. - Source: PubMed
Publication date: 2024/11/26
Ngok SreymeanYann RemChey Chan OeurnLiu XianjieWillander MagnusNur Omer - While increased mutation rates typically have negative consequences in multicellular organisms, hypermutation can be advantageous for microbes adapting to the environment. Previously, we identified two hypermutator clinical isolates that rapidly develop drug resistance due to transposition of a retrotransposon, Cnl1. Cnl1-mediated hypermutation is caused by a nonsense mutation in a gene encoding an RNA interference (RNAi) component, , combined with a tremendous transposon burden. To elucidate adaptive mechanisms following RNAi loss, two bioinformatic pipelines were developed to identify RNAi loss-of-function (LOF) mutations in a collection of 387 sequenced isolates. Remarkably, several RNAi-loss isolates were identified that are not hypermutators and have not accumulated transposons. To test whether these RNAi LOF mutations can cause hypermutation, the mutations were introduced into a nonhypermutator strain with a high transposon burden, which resulted in a hypermutator phenotype. To further investigate whether RNAi-loss isolates can become hypermutators, in vitro passaging was performed. Although no hypermutators were found in two RNAi-loss strains after short-term passage, hypermutation was observed in a passaged strain with an increased transposon burden. Consistent with a two-step evolution, when an RNAi-loss isolate was crossed with an isolate containing a high Cnl1 burden, F1 hypermutator progeny inheriting a high transposon burden were identified. In addition to Cnl1 transpositions, insertions of a gigantic DNA transposon KDZ1 (~11 kb) contributed to hypermutation in the progeny. Our results suggest that RNAi loss is relatively common (7/387, ~1.8%) and enables distinct evolutionary trajectories: hypermutation following transposon accumulation or survival without hypermutation. - Source: PubMed
Publication date: 2024/11/13
Huang JunLarmore Connor JPriest Shelby JXu ZiyanDietrich Fred SYadav VikasMagwene Paul MSun ShengHeitman Joseph