ZNF404 may be involved in transcriptional regulation.
- Known as:
- ZNF404 involved transcriptional regulation.
- Catalog number:
- 25-039
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ZNF404 may involved transcriptional regulation.
Related genes to: ZNF404 may be involved in transcriptional regulation.
- Gene:
- ZNF404 NIH gene
- Name:
- zinc finger protein 404
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-04
- Date modifiied:
- 2014-11-19
Related products to: ZNF404 may be involved in transcriptional regulation.
*Please allow 3-5 days for delivery time.* RAIDD (RIP-associated ICH-1 homologous protein with a death domain) is an adaptor molecule that mediates the action of cysteine proteases involved in apoptos11-zinc finger protein,CCCTC-binding factor,Chicken,CTCF,CTCFL paralog,Gallus gallus,Transcriptional repressor CTCF11-zinc finger protein,CCCTC-binding factor,CTCF,CTCFL paralog,Homo sapiens,Human,Transcriptional repressor CTCF11-zinc finger protein,CCCTC-binding factor,Ctcf,CTCFL paralog,Mouse,Mus musculus,Transcriptional repressor CTCF11-zinc finger protein,CCCTC-binding factor,Ctcf,CTCFL paralog,Rat,Rattus norvegicus,Transcriptional repressor CTCF110V-to-100V Voltage Transformer 5 A capacity. Net price (not negotiatable). Voltage transformer may be locally prepared, instead of purchasing from Atto.110V-to-100V Voltage Transformer 5 A capacity. Net price (not negotiatable). Voltage transformer may be locally prepared, instead of purchasing from Atto.14-3-3 sigma Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months.14-3-3 tau Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months.17-beta-hydroxysteroid dehydrogenases, such as HSD17B14, are primarily involved in metabolism of steroids at the C17 position and also of other substrates, such as fatty acids, prostaglandins, and xen240V-to-100V Voltage Transformer 5 A capacity. Net price (not negotiatable). Voltage transformer may be locally prepared, instead of purchasing from Atto.240V-to-100V Voltage Transformer 5 A capacity. Net price (not negotiatable). Voltage transformer may be locally prepared, instead of purchasing from Atto.3 prime Exonuclease Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months.39873 Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months.39876 Peptide Please note that this peptide has a delivery time of approximately 3 weeks. If the peptide is out of stock, the delivery time may take up to 1-3 months. Related articles to: ZNF404 may be involved in transcriptional regulation.
- Fused-in sarcoma (FUS) gene mutations have been implicated in amyotrophic lateral sclerosis (ALS). This study aimed to investigate the impact of FUS mutations (R521H and P525L) on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Using RNA sequencing (RNA Seq), we characterized differentially expressed genes (DEGs) and differentially expressed lncRNAs (DELs) and subsequently predicted lncRNA-mRNA target pairs (TAR pairs). Our results show that FUS mutations significantly altered the expression profiles of mRNAs and lncRNAs in iPSCs. Using this large dataset, we identified and verified six key differentially regulated TAR pairs in iPSCs that were also altered in iMNs. These target transcripts included: GPR149, NR4A, LMO3, SLC15A4, ZNF404, and CRACD. These findings indicated that selected mutant FUS-induced transcriptional alterations persist from iPSCs into differentiated iMNs. Functional enrichment analyses of DEGs indicated pathways associated with neuronal development and carcinogenesis as likely altered by these FUS mutations. Furthermore, ingenuity pathway analysis (IPA) and GO network analysis of lncRNA-targeted mRNAs indicated associations between RNA metabolism, lncRNA regulation, and DNA damage repair. Our findings provide insights into potential molecular mechanisms underlying the pathophysiology of ALS-associated FUS mutations and suggest potential therapeutic targets for the treatment of ALS. - Source: PubMed
Publication date: 2023/10/16
Provasek Vincent EKodavati ManoharGuo WentingWang HaiboBoldogh IstvanVan Den Bosch LudoBritz GavinHegde Muralidhar L - () gene mutations have been implicated in amyotrophic lateral sclerosis (ALS). This study aimed to investigate the impact of FUS mutations (R521H and P525L) on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Using RNA sequencing (RNA Seq), we characterized differentially expressed genes (DEGs), differentially expressed lncRNAs (DELs), and subsequently predicted lncRNA-mRNA target pairs (TAR pairs). Our results show that FUS mutations significantly altered expression profiles of mRNAs and lncRNAs in iPSCs. We identified key differentially regulated TAR pairs, including LMO3, TMEM132D, ERMN, GPR149, CRACD, and ZNF404 in mutant FUS iPSCs. We performed reverse transcription PCR (RT-PCR) validation in iPSCs and iMNs. Validation confirmed RNA-Seq findings and suggested that mutant FUS-induced transcriptional alterations persisted from iPSCs into differentiated iMNs. Functional enrichment analyses of DEGs indicated pathways associated with neuronal development and carcinogenesis that were likely altered by FUS mutations. Ingenuity Pathway Analysis (IPA) and GO network analysis of lncRNA-targeted mRNAs indicated associations related to RNA metabolism, lncRNA regulation, and DNA damage repair. Our findings provide insights into the molecular mechanisms underlying the pathophysiology of ALS-associated FUS mutations and suggest potential therapeutic targets for the treatment of ALS. - Source: PubMed
Publication date: 2023/06/27
Provasek Vincent EKodavati ManoharGuo WentingWang HaiboBoldogh IstvanVan Den Bosch LudoBritz GavinHegde Muralidhar - The present study explored the effects of ascorbic-acid (AA)/retinol and timed inflammation on the stemness, the regenerative potential, and the transcriptomics profile of gingival mesenchymal stem/progenitor cells' (G-MSCs). STRO-1 (mesenchymal stem cell marker) immuno-magnetically sorted G-MSCs were cultured in basic medium (control group), in basic medium with IL-1β (1 ng/mL), TNF-α (10 ng/mL) and IFN-γ (100 ng/mL, inflammatory-medium), in basic medium with AA (250 µmol/L) and retinol (20 µmol/L) (AA/retinol group) or in inflammatory medium with AA/retinol (inflammatory/AA/retinol group; = 5/group). The intracellular levels of phosphorylated and total β-Catenin at 1 h, the expression of stemness genes over 7 days, the number of colony-forming units (CFUs) as well as the cellular proliferation aptitude over 14 days, and the G-MSCs' multilineage differentiation potential were assessed. Next-generation sequencing was undertaken to elaborate on up-/downregulated genes and altered intracellular pathways. G-MSCs demonstrated all mesenchymal stem/progenitor cells characteristics. Controlled inflammation with AA/retinol significantly elevated ( < 0.05). The AA/retinol-mediated reduction in intracellular phosphorylated β-Catenin was restored through the effect of controlled inflammation ( < 0.05). Cellular proliferation was highest in the AA/retinol group ( < 0.05). AA/retinol counteracted the inflammation-mediated reduction in G-MSCs' clonogenic ability and CFUs. Amplified chondrogenic differentiation was observed in the inflammatory/AA/retinol group. At 1 and 3 days, the differentially expressed genes were associated with development, proliferation, and migration (, , , , , , ), survival (, , ), differentiation and mineral absorption (, , , , , ), inflammation and MHC-II antigen processing (, , ) and intracellular pathway activation (, ). Less as well as more genes were activated the longer the G-MSCs remained in the inflammatory medium or AA/retinol, respectively. Combined, current results point at possibly interesting interactions between controlled inflammation or AA/retinol affecting stemness, proliferation, and differentiation attributes of G-MSCs. - Source: PubMed
Publication date: 2021/11/25
Fawzy El-Sayed Karim MBittner AmiraSchlicht KristinaMekhemar MohamedEnthammer KimHöppner MarcEs-Souni MarthaSchulz JulianeLaudes MatthiasGraetz ChristianDörfer Christof ESchulte Dominik M - Genome-wide association studies (GWAS) have discovered thousands loci associated with disease risk and quantitative traits, yet most of the variants responsible for risk remain uncharacterized. The majority of GWAS-identified loci are enriched for non-coding single-nucleotide polymorphisms (SNPs) and defining the molecular mechanism of risk is challenging. Many non-coding causal SNPs are hypothesized to alter transcription factor (TF) binding sites as the mechanism by which they affect organismal phenotypes. We employed an integrative genomics approach to identify candidate TF binding motifs that confer breast cancer-specific phenotypes identified by GWAS. We performed de novo motif analysis of regulatory elements, analyzed evolutionary conservation of identified motifs, and assayed TF footprinting data to identify sequence elements that recruit TFs and maintain chromatin landscape in breast cancer-relevant tissue and cell lines. We identified candidate causal SNPs that are predicted to alter TF binding within breast cancer-relevant regulatory regions that are in strong linkage disequilibrium with significantly associated GWAS SNPs. We confirm that the TFs bind with predicted allele-specific preferences using CTCF ChIP-seq data. We used The Cancer Genome Atlas breast cancer patient data to identify ANKLE1 and ZNF404 as the target genes of candidate TF binding site SNPs in the 19p13.11 and 19q13.31 GWAS-identified loci. These SNPs are associated with the expression of ZNF404 and ANKLE1 in breast tissue. This integrative analysis pipeline is a general framework to identify candidate causal variants within regulatory regions and TF binding sites that confer phenotypic variation and disease risk. - Source: PubMed
Publication date: 2017/09/28
Liu YunxianWalavalkar Ninad MDozmorov Mikhail GRich Stephen SCivelek MeteGuertin Michael J - The genome-wide association studies (GWAS) have enabled us in identifying different breast cancer (BC) susceptibility loci. However, majority of these are non-coding variants with no annotated biological function. We investigated such 78 noncoding genome wide associated SNPs of BC and further expanded the list to 2,162 variants with strong linkage-disequilibrium (LD, r ≥0.8). Using multiple publically available algorithms such as CADD, GWAVA, and FATHAMM, we classified all these variants into deleterious, damaging, or benign categories. Out of total 2,241 variants, 23 (1.02%) variants were extreme deleterious (rank 1), 70 (3.12%) variants were deleterious (rank 2), and 1,937 (86.43%) variants were benign (rank 3). The results show 14% of lead or associated variants are under strong negative selection (GERP++ RS ≥2), and ∼22% are under balancing selection (Tajima's D score >2) in CEU population of 1KGP-the regions being positively selected (GERP++ RS <0) in mammalian evolution. The expression quantitative trait loci of highest deleteriously ranked genes were tested on relevant adipose and breast tissues, the results of which were extended for protein expression on breast tissues. From the concordance analysis of ranking system of GWAVA, CADD, and FATHMM, eQTL and protein expression, we identified the deleterious SNPs localized in STXBP4 and ZNF404 genes which might play a role in BC development by dysregulating its gene expression. This simple approach will be easier to implement and to prioritize large scale GWAS data for variety of diseases and link to the potentially unrecognized functional roles of genes. J. Cell. Biochem. 118: 4296-4307, 2017. © 2017 Wiley Periodicals, Inc. - Source: PubMed
Publication date: 2017/05/25
Masoodi Tariq AhmadBanaganapalli BabajanVaidyanathan VenkateshTalluri Venkateswar RShaik Noor A