Ask about this productRelated genes to: ZNF778 antibody
- Gene:
- ZNF778 NIH gene
- Name:
- zinc finger protein 778
- Previous symbol:
- -
- Synonyms:
- FLJ31875
- Chromosome:
- 16q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-15
- Date modifiied:
- 2019-04-23
Related products to: ZNF778 antibody
Related articles to: ZNF778 antibody
- Rare genetic variants that affect host defense against SARS-CoV-2 may contribute to COVID-19 progression, helping to explain severe or fatal cases in young and middle-aged patients. This study aimed to identify rare genetic variants potentially implicated in life-threatening COVID-19 in a cohort of Brazilian patients aged 18 to 60, with no prior history of health issues, who required intensive care unit admission (n = 161). Whole genome sequencing was performed, followed by a prioritization approach for rare variants in loci previously associated with severe COVID-19. A total of 104 rare and potentially deleterious variants were identified in 79 genes. Ultra-rare variants in MUC5AC, IFNA10, ZNF778, and PTOV1 were the most frequently observed. We report 17 novel variants, including those likely pathogenic or indicating strong loss-of-function (LoF) intolerance. Patients carrying prioritized rare variants had a significantly higher incidence of acute respiratory distress syndrome (ARDS) (p = 0.027, OR = 2.59). Additionally, patients with variants in highly LoF-intolerant genes had a fourfold higher risk of death (p = 0.0084, OR = 4.04). To date, this is the first genomic analysis of previously healthy young and middle-aged Latin American patients with severe COVID-19. Our findings highlight the importance of identifying population-specific genetic risk factors. - Source: PubMed
Publication date: 2025/07/02
Rocha Gabriela DiasOliveira Pablo Rafael Silveirade Oliveira Sá Marcus Villander Barrosde Lima Campos TúlioGaldino Galisa Steffany LarissaSilva Andreia SoaresMoura Patriciade São Pedro Raquel BispoTavares Natália MachadoBoaventura Viviane SampaioNunes SaraBonyek-Silva IcaroCaldas Juliana RibeiroRoma Eric HenriqueAlmeida Jorge ReisSilva Andrea AliceBaccin Tatianade Castro Andrea CauduroVallinoto Antônio Carlos Rosarioda Silva RosileneDos Santos Eduardo José MeloGarcia Cristiana CoutoSlhessarenko Renata Dezengrinida Costa Armstrong Andersondo Carmo Rodrigo FelicianoVasconcelos Luydson Richardson Silva - In multiple malignant tumors, circular RNAs (circRNAs) are believed to play a crucial role. Our prior results demonstrated that circ_ZNF778_006 was significantly increased in esophageal squamous cell carcinoma (ESCC) tissues, but the roles of circ_ZNF778_006 in ESCC is still not clear. The expression of circ_ZNF778_006 was compared in different pathological grades of ESCC. And the expression levels of circ_ZNF778_006, miR-18b-5p, HIF-1α were analyzed by qRT-PCR and Western blot, respectively. Plasmid transfection techniques were applied to prepare ESCC cells with silenced or overexpressed genes (CircZNF778_006, miR-18b-5p). The CCK8 kit was used to determine cell proliferation, and the Transwell assay was used to measure the migration and invasion. The effects of circ_ZNF778_006 on tumor growth was investigated in vivo. Furthermore, luciferase reporter gene assay and RNA-binding protein immunoprecipitation (RIP) were performed to verify the targeting relationship between miR-18b-5p and circZNF778_006, miR-18b-5p and HIF-1α. The expression of circ_ZNF778_006 was positively correlated with pathological grade in ESCC. Circ_ZNF778_006 significantly inhibited sensitivity to 5-fluorouracil & cisplatin. It could promote the proliferation, invasion, migration in ESCC cells and accelerated tumor growth in vivo. Furthermore, circ_ZNF778_006 could upregulate the expression of HIF-1α via sponing miR-18b-5p. Circ_ZNF778_006 promoted ESCC progression by upregulating HIF-1α expression via sponging miR-18b-5p. - Source: PubMed
Publication date: 2023/11/08
Si XianzheSu XinchengLin WeijieXu JieHuang WenboChen FengHuang ZhijunLin JianqingChen Zhiyao - RAS proteins are GTPases that lie upstream of a signaling network impacting cell fate determination. How cells integrate RAS activity to balance proliferation and cellular senescence is still incompletely characterized. Here, we identify ZNF768 as a phosphoprotein destabilized upon RAS activation. We report that ZNF768 depletion impairs proliferation and induces senescence by modulating the expression of key cell cycle effectors and established p53 targets. ZNF768 levels decrease in response to replicative-, stress- and oncogene-induced senescence. Interestingly, ZNF768 overexpression contributes to bypass RAS-induced senescence by repressing the p53 pathway. Furthermore, we show that ZNF768 interacts with and represses p53 phosphorylation and activity. Cancer genomics and immunohistochemical analyses reveal that ZNF768 is often amplified and/or overexpressed in tumors, suggesting that cells could use ZNF768 to bypass senescence, sustain proliferation and promote malignant transformation. Thus, we identify ZNF768 as a protein linking oncogenic signaling to the control of cell fate decision and proliferation. - Source: PubMed
Publication date: 2021/08/17
Villot RomainPoirier AudreyBakan InanBoulay KarineFernández ErlindaDevillers RomainGama-Braga LucianoTribouillard LauraGagné AndréanneDuchesne ÉmaCaron DanielleBérubé Jean-SébastienBérubé Jean-ChristopheCoulombe YanOrain MichèleGélinas YvesGobeil StéphaneBossé YohanMasson Jean-YvesElowe SabineBilodeau SteveManem VenkataJoubert PhilippeMallette Frédérick ALaplante Mathieu - Mammalian-wide interspersed repeats (MIRs) are retrotransposed elements of mammalian genomes. Here, we report the specific binding of zinc finger protein ZNF768 to the sequence motif GCTGTGTG (N20) CCTCTCTG in the core region of MIRs. ZNF768 binding is preferentially associated with euchromatin and promoter regions of genes. Binding was observed for genes expressed in a cell type-specific manner in human B cell line Raji and osteosarcoma U2OS cells. Mass spectrometric analysis revealed binding of ZNF768 to Elongator components Elp1, Elp2 and Elp3 and other nuclear factors. The N-terminus of ZNF768 contains a heptad repeat array structurally related to the C-terminal domain (CTD) of RNA polymerase II. This array evolved in placental animals but not marsupials and monotreme species, displays species-specific length variations, and possibly fulfills CTD related functions in gene regulation. We propose that the evolution of MIRs and ZNF768 has extended the repertoire of gene regulatory mechanisms in mammals and that ZNF768 binding is associated with cell type-specific gene expression. - Source: PubMed
Rohrmoser MichaelaKluge MichaelYahia YousraGruber-Eber AnitaMaqbool Muhammad AhmadForné IgnasiKrebs StefanBlum HelmutGreifenberg Ann KatrinGeyer MatthiasDescostes NicolasImhof AxelAndrau Jean-ChristopheFriedel Caroline CEick Dirk - 16q24 deletion involving the ANKRD11 gene, ranging from 137 kb to 2 Mb, have been associated with a microdeletion syndrome characterized by variable cognitive impairment, autism spectrum disorder, facial dysmorphisms with dental anomalies, brain abnormalities essentially affecting the corpus callosum and short stature. On the other hand, patients carrying either deletions encompassing solely ANKRD11 or its loss-of-function variants were reported in association with the KBG syndrome, characterized by a very similar phenotype, including mild-to-moderate intellectual disability, short stature and macrodontia of upper incisors, with inter and intrafamilial variability. To assess whether the haploinsufficiency of ANKRD11-flanking genes, such as ZFPM1, CDH15 and ZNF778, contributed to either the severity of the neurological impairment or was associated with other clinical features, we collected 12 new cases with a 16q24.2q24.3 deletion (de novo in 11 cases), ranging from 343 kb to 2.3 Mb. In 11 of them, the deletion involved the ANKRD11 gene, whereas in 1 case only flanking genes upstream to it were deleted. By comparing the clinical and genetic features of our patients with those previously reported, we show that the severity of the neurological phenotype and the frequency of congenital heart defects characterize the deletions that, besides ANKRD11, contain ZFPM1, CDH15 and ZNF778 as well. Moreover, the presence of thrombocytopenia and astigmatism should be taken into account to distinguish between 16q24 microdeletion syndrome and KBG syndrome. The single patient not deleted for ANKRD11, whose phenotype is characterized by milder psychomotor delay, cardiac congenital malformation, thrombocytopenia and astigmatism, confirms all this data. - Source: PubMed
Publication date: 2017/04/19
Novara FrancescaRinaldi BerardoSisodiya Sanjay MCoppola AntoniettaGiglio SabrinaStanzial FrancoBenedicenti FrancescoDonaldson AlanAndrieux JorisStapleton RachelWeber AstridReho Paolovan Ravenswaaij-Arts ConnyKerstjens-Frederikse Wilhelmina SVermeesch Joris RobertDevriendt KoenraadBacino Carlos ADelahaye AndréeMaas S MIolascon AchilleZuffardi Orsetta