Ask about this productRelated genes to: ZNF554 antibody
- Gene:
- ZNF554 NIH gene
- Name:
- zinc finger protein 554
- Previous symbol:
- -
- Synonyms:
- FLJ34817
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-15
- Date modifiied:
- 2014-11-19
Related products to: ZNF554 antibody
Related articles to: ZNF554 antibody
- Uterine corpus endometrial carcinoma (UCEC), a kind of gynecologic malignancy, poses a significant risk to women's health. The precise mechanism underlying the development of UCEC remains elusive. Zinc finger protein 554 (ZNF554), a member of the Krüppel-associated box domain zinc finger protein superfamily, was reported to be dysregulated in various illnesses, including malignant tumors. This study aimed to examine the involvement of ZNF554 in the development of UCEC. - Source: PubMed
Publication date: 2024/04/15
Zhu Cheng-ChengSun Heng-LiangLong Teng-FeiLyu Yuan-YuanLiu Jiang-LiNi Guan-Tai - Fetal growth restriction (FGR) is one of the most common complications of an abnormal pregnancy. Placental dysplasia has been established as a significant contributing factor to FGR. Zinc finger protein 554 (ZNF554) is a member of the Krüppel-associated box domain zinc finger protein subfamily, primarily expressed in the placenta and essential for maintaining normal pregnancy outcomes. However, its precise role in FGR remains uncertain. In this study, we confirmed that ZNF554 was low expressed in the placenta of the FGR pregnancy. To further elucidate the impact of ZNF554 on trophoblasts, we conducted experiments using siRNA and overexpression plasmids on HTR8/SVneo and JEG3 cells. Our findings revealed that silencing ZNF554 increased apoptosis and inhibited migration and invasion, while overexpression reduced apoptosis and promoted migration and invasion. Notably, ZNF554 knockdown decreased cellular antioxidant capacity and elevated the production of reactive oxygen species (ROS). Conversely, ZNF554 activated the nuclear factor E2-related factor 2 (NRF2) signaling pathway, exerting its antioxidant effects. Additionally, ZNF554 knockdown promoted cellular autophagy by suppressing P62 and enhancing LC3-II/LC3-I expression. Importantly, the antioxidant N-acetylcysteine (NAC) partially mitigated the impact of ZNF554 knockdown on mitochondrial ROS in trophoblast cells and subsequent effects on cellular autophagy and apoptosis. In conclusion, our results suggest that ZNF554 plays a pivotal role in modulating trophoblast cell invasion and may serve as a prognostic marker and potential therapeutic target for FGR. - Source: PubMed
Publication date: 2023/09/30
Guo YanyanHuang ChuyiXu CailingQiu LiyanYang Fang - Zinc finger protein 554 (ZNF554), a member of the Krüppel-associated box domain zinc finger protein subfamily, is predominantly expressed in the brain and placenta in humans. Recently, we unveiled that ZNF554 regulates trophoblast invasion during placentation and its decreased expression leads to the early pathogenesis of preeclampsia. Since ZNF proteins are immensely implicated in the development of several tumors including malignant tumors of the brain, here we explored the pathological role of ZNF554 in gliomas. e examined the expression of ZNF554 at mRNA and protein levels in normal brain and gliomas, and then we searched for genome-wide transcriptomic changes in U87 glioblastoma cells transiently overexpressing . Immunohistochemistry of brain tissues in our cohort ( = 62) and analysis of large TCGA RNA-Seq data ( = 687) of control, oligodendroglioma, and astrocytoma tissues both revealed decreased expression of towards higher glioma grades. Furthermore, low expression was associated with shorter survival of grade III and IV astrocytoma patients. Overexpression of in U87 cells resulted in differential expression, mostly downregulation of 899 genes. The "PI3K-Akt signaling pathway", known to be activated during glioma development, was the most impacted among 116 dysregulated pathways. Most affected pathways were cancer-related and/or immune-related. Congruently, cell proliferation was decreased and cell cycle was arrested in -transfected glioma cells. These data collectively suggest that ZNF554 is a potential tumor suppressor and its decreased expression may lead to the loss of oncogene suppression, activation of tumor pathways, and shorter survival of patients with malignant glioma. - Source: PubMed
Publication date: 2020/08/11
Balogh AndreaReiniger LillaHetey SzabolcsKiraly PeterToth EszterKaraszi KatalinJuhasz KataGelencser ZsoltZvara AgnesSzilagyi AndrasPuskas Laszlo GMatko JanosPapp ZoltanKovalszky IlonaJuhasz CsabaThan Nandor Gabor - Preeclampsia is a disease of the mother, fetus, and placenta, and the gaps in our understanding of the complex interactions among their respective disease pathways preclude successful treatment and prevention. The placenta has a key role in the pathogenesis of the terminal pathway characterized by exaggerated maternal systemic inflammation, generalized endothelial damage, hypertension, and proteinuria. This of preeclampsia may be triggered by distinct underlying mechanisms that occur at early stages of pregnancy and induce different phenotypes. To gain insights into these molecular pathways, we employed a systems biology approach and integrated different "omics," clinical, placental, and functional data from patients with distinct phenotypes of preeclampsia. First trimester maternal blood proteomics uncovered an altered abundance of proteins of the renin-angiotensin and immune systems, complement, and coagulation cascades in patients with term or preterm preeclampsia. Moreover, first trimester maternal blood from preterm preeclamptic patients dysregulated trophoblastic gene expression. Placental transcriptomics of women with preterm preeclampsia identified distinct gene modules associated with maternal or fetal disease. Placental "virtual" liquid biopsy showed that the dysregulation of these disease gene modules originates during the first trimester. experiments on hub transcription factors of these gene modules demonstrated that DNA hypermethylation in the regulatory region of leads to gene down-regulation and impaired trophoblast invasion, while and up-regulation sensitizes the trophoblast to ischemia, hallmarks of preterm preeclampsia. In summary, our data suggest that there are distinct maternal and placental disease pathways, and their interaction influences the clinical presentation of preeclampsia. The activation of maternal disease pathways can be detected in all phenotypes of preeclampsia earlier and upstream of placental dysfunction, not only downstream as described before, and distinct placental disease pathways are superimposed on these maternal pathways. This is a paradigm shift, which, in agreement with epidemiological studies, warrants for the central pathologic role of preexisting maternal diseases or perturbed maternal-fetal-placental immune interactions in preeclampsia. The description of these novel pathways in the "molecular phase" of preeclampsia and the identification of their hub molecules may enable timely molecular characterization of patients with distinct preeclampsia phenotypes. - Source: PubMed
Publication date: 2018/08/08
Than Nandor GaborRomero RobertoTarca Adi LaurentiuKekesi Katalin AdriennaXu YiXu ZhonghuiJuhasz KataBhatti GauravLeavitt Ron JoshuaGelencser ZsoltPalhalmi JanosChung Tzu HungGyorffy Balazs AndrasOrosz LaszloDemeter AmandaSzecsi AnettHunyadi-Gulyas EvaDarula ZsuzsannaSimor AttilaEder KatalinSzabo SzilviaTopping VanessaEl-Azzamy HaidyLaJeunesse ChristopherBalogh AndreaSzalai GaborLand SusanTorok OlgaDong ZhongKovalszky IlonaFalus AndrasMeiri HamutalDraghici SorinHassan Sonia SChaiworapongsa TinnakornKrispin ManuelKnöfler MartinErez OfferBurton Graham JKim Chong JaiJuhasz GaborPapp Zoltan