Ask about this productRelated genes to: ZNF714 antibody
- Gene:
- ZNF714 NIH gene
- Name:
- zinc finger protein 714
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p12
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-17
- Date modifiied:
- 2016-07-26
Related products to: ZNF714 antibody
Related articles to: ZNF714 antibody
- Cardiometabolic phenotypes such as obesity and impaired insulin action are key determinants of type 2 diabetes (T2D). Growing evidence highlights the postprandial state as a critical window in metabolic regulation, where epigenetic mechanisms, particularly DNA methylation in insulin-sensitive tissues, may play pivotal roles. However, their dynamics across prandial states in subcutaneous adipose tissue (SAT) remain unclear. We analyzed genome-wide DNA methylation in paired fasting and postprandial SAT biopsies from 29 asymptomatic, drug-naïve individuals classified as controls ( = 8), prediabetes = 9), or T2D ( = 12). Postprandial samples followed a standardized mixed-meal test. DNA methylation was quantified using the Illumina MethylationEPIC array and analyzed through the Chip Analysis Methylation Pipeline (ChAMP) pipeline. Differential methylation was more pronounced postprandially, especially in the T2D group. After adjusting for age and sex, 4599 differentially methylated CpG sites (DMCs) were identified, with increased hypermethylation in T2D. A total of 130 DMCs across 99 genes, including , , , and , were shared by prediabetes and T2D groups. Over-representation analysis revealed 202 enriched pathways related to insulin resistance, AMPK signaling, and immune responses. Additionally, 110 Differentially Methylated Regions (DMRs), including and , were detected. These findings reveal early, prandial-dependent epigenetic alterations in SAT that precede overt dysglycemia, offering insights into personalized prevention in T2D. - Source: PubMed
Publication date: 2025/11/22
Escalante-Araiza FabiolaMartínez-Hernández AngélicaGarcía-Ortiz HumbertoHuerta-Ávila EiraVillafan-Bernal José RafaelContreras-Cubas CeciliaCenteno-Cruz FedericoGemm Family Study Nava-González Edna JCarrillo-Ruiz José DamiánRodriguez-Ayala ErnestoBastarrachea Raúl ABarajas-Olmos FranciscoOrozco Lorena - Low birth weight in newborns is of multifactorial origin (fetal, maternal, placental, and environmental factors), and in one-third of cases, the cause is of unknown origin, with high infant morbidity and mortality. The main treatment for regaining weight and height in children with low birth weight is the application of growth hormones. However, their role as a protective factor to prevent an increase in body composition and the development of metabolic diseases is still poorly understood. : A case-control study was conducted in a cohort of patients consulted at the CES Pediatric Endocrinology Clinic, Medellín, Colombia, between 2008 and 2018. We evaluated sociodemographic and clinical variables. Additionally, the identification of differential patterns of genomic methylation between cases (treated with growth hormone) and controls (without growth hormone treatment) was performed. The groups were compared using Fisher's exact test for qualitative variables and Student's -test for the difference in means in independent samples. The correlation was evaluated with the Pearson coefficient. Regarding clinical manifestations, body mass index (BMI) was higher in children who did not receive growth hormone treatment, higher doses of growth hormone treatment helped reduce body mass index (R: -0.21, and = 0.067), and the use of growth hormone was related to a decrease in triglyceride blood concentrations ( = 0.06); these results tended towards significance. Regarding genome-wide methylation patterns, the following genes were found to be hypermethylated: , and . Meanwhile, the following genes were found hypomethylated: , and . Using growth hormone as a treatment in SGA newborns helps regain weight and height. Additionally, it could be a protective factor against the increase in adolescent body composition. - Source: PubMed
Publication date: 2025/05/23
Velásquez Juan M AlfaroVásquez Trespalacios Elsa MariaUrrego RodrigoArroyave Toro María CMontilla Velásquez María Del PilarSoto Cecilia Maria DíazVélez Juan C ZuluagaJaramillo Henríquez VerónicaFlórez Jorge Emilio SalazarMonroy Fernando PPalacio Mosquera Hernando AlirioVélez Gómez SaraPelaez Sánchez Ronald Guillermo - Despite the ongoing progress in diagnosis and treatments, cancer remains a threat to more than one-third of the human population. The emerging data indicate that many Krüppel-associated box zinc finger proteins (KRAB-ZNF) belonging to a large gene family may be involved in carcinogenesis. Our previous study identified Zinc Finger Protein 714 (ZNF714), a KRAB-ZNF gene of unknown function, as being commonly overexpressed in many tumors, pointing to its hypothetical oncogenic role. Here, we harnessed The Cancer Genome Atlas (TCGA)-centered databases and performed functional studies with transcriptomic and methylomic profiling to explore ZNF714 function in cancer. Our pan-cancer analyses confirmed frequent ZNF714 overexpression in multiple tumors, possibly due to regional amplification, promoter hypomethylation, and Nuclear Transcription Factor Y Subunit Beta (NFYB) signaling. We also showed that ZNF714 expression correlates with tumor immunosuppressive features. The in vitro studies indicated that ZNF714 expression positively associates with proliferation, migration, and invasion. The transcriptomic analysis of ZNF714 knocked-down cells demonstrated deregulation of cell adhesion, migration, proliferation, apoptosis, and differentiation. Importantly, we provided evidence that ZNF714 negatively regulates the expression of several known TSGs indirectly via promoter methylation. However, as ZNF714 did not show nuclear localization in our research model, the regulatory mechanisms exerted by ZNF714 require further investigation. In conclusion, our results reveal, for the first time, that ZNF714 may support pro-oncogenic features in lung cancer cells. - Source: PubMed
Publication date: 2023/10/24
Oleksiewicz UrszulaMachnik MartaSobocińska JoannaMolenda SaraOlechnowicz AnnaFlorczak AnnaSmolibowski MikołajKaczmarek Mariusz - Suicide is multifactorial and polygenic phenotype, affected by environmental and genetic factors. Among epigenetic mechanisms, miRNAs have been studied, but so far no very concise results exist. To overcome limitations of candidate miRNA and whole genome sequencing approaches, we created an in silico analysis algorithm that would help select the best suitable miRNAs that target the most interesting genes associated with suicidality. We used databases/web algorithms DIANA microT, miRDB, miRmap, miRWalk, and TargetScan and candidate genes , , , , , and . Based on a prediction algorithm, we have chosen miRNAs that are targeting regulation of the genes listed, and are at the same time being expressed in the brain. The highest ranking scores were obtained for hsa-miR-4516, hsa-miR-3135b, hsa-miR-124-3p, hsa-miR-129-5p, hsa-miR-27b-3p, hsa-miR-381-3p, hsa-miR-4286. Expression of these miRNAs was tested in the brain tissue of 40 suicide completers and controls, and hsa-miR-4516 and hsa-miR-381-3p showed a trend for statistical significance. We also checked the expression of the target genes of these miRNAs, and for expression was lower in suicide completers compared to controls, which is in accordance with the available literature results. To determine the miRNAs that are most suitable for further suicidality research, more studies, combining in silico analysis and wet lab experiments, should be performed. - Source: PubMed
Publication date: 2022/03/23
Videtič Paska AljaAlič UrbanZupanc TomažKouter Katarina - Ovarian cancer is a disease that is generally diagnosed at an advanced stage, and has poor survival. Monozygotic (MZ) twins are considered to be good research models for investigating the epigenetic changes associated with diseases. In the present study, the involvement of epigenetic mechanisms in ovarian cancer etiology were evaluated using the MZ twin model. Whole-genome methylation patterns were investigated in a gene mutation-carrying family comprising MZ twins, only one of whom had ovarian cancer, and other healthy siblings. Whole-genome methylation patterns were assessed in peripheral blood DNA using Infinium MethylationEPIC BeadChips on an Illumina iScan device. The hypermethylated and hypomethylated genes were detected between cases and controls in four different comparison groups in order to evaluate the differences in methylation levels according to cancer diagnosis and mutation status. The obtained results showed that the differential methylations in 12 different genes, namely PR/SET domain 6, cytochrome B5 reductase 4, , clustered mitochondria homolog, RB-binding protein 7, chromatin repair factor, ankyrin repeat domain 23, RIB43A domain with coiled-coils 1 and , were associated with ovarian cancer. Biological functional analysis of the genes detected in the study using the PANTHER classification system revealed that they have roles in biological processes including 'biologic adhesion', 'regulation', 'cellular components organization', 'biogenesis', 'immune system functioning', 'metabolic functioning' and 'localization'. Overall, the present study suggested that epigenetic differences, such as methylation status, could be used as a non-invasive biological markers for the early diagnosis and follow-up of ovarian cancer. - Source: PubMed
Publication date: 2020/10/14
Erdogan Ozge SukruogluTuncer Seref BugraKilic SedaOdemis Demet AkdenizTurkcan Gozde KuruCelik BetulAvsar MukaddesYazici Hulya