Ask about this productRelated genes to: ZZZ3 Blocking Peptide
- Gene:
- ZZZ3 NIH gene
- Name:
- zinc finger ZZ-type containing 3
- Previous symbol:
- -
- Synonyms:
- DKFZP564I052, ATAC1
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-02-12
Related products to: ZZZ3 Blocking Peptide
Related articles to: ZZZ3 Blocking Peptide
- Adoptive transfer of tumor-infiltrating lymphocytes (TIL) is effective in melanoma and selected solid tumors, but its potential in pancreatic ductal adenocarcinoma (PDAC) remains largely unexplored. We report a 39-year-old male with metastatic PDAC involving lung, peritoneal, liver, and lymph node who received three sequential infusions of TIL expanded ex vivo with IL-2/IL-15/IL-21 from a lung metastasis. Each infusion followed low-dose lymphodepletion and IL-2 support. The patient achieved stable disease after the first infusion and a partial response after the second along with reductions in serum CA19-9. Genome sequencing revealed substantial inter-tumoral heterogeneity, with mutations in ITGB2, C1QTNF3, CDK9, TMEM200C, FHOD1 and ZZZ3 impacting TIL infiltration and clinical response. RNA-seq showed that responding lesions were enriched for inflammatory and tumor-specific programs, displayed enrichment of T-cell activation transcripts and had reduced infiltration of cancer-associated fibroblasts. TCR sequencing confirmed the robust infiltration of TIL-derived CD8+ clonotypes, while functional assays demonstrated a polyclonal recognition of patient-derived somatic mutations and cytotoxicity against autologous tumor lines. Single-cell TCR mapping further validated the dominance of tumor-specific CD8+ clonotypes in responding lesions. This case demonstrates the feasibility and immunological activity of TIL therapy in PDAC, while underscoring the impact of spatial tumor heterogeneity on therapeutic outcomes. - Source: PubMed
Publication date: 2026/03/04
Arruda Lucas C MKarbach JuliaKiselicki DraganSinelnikov EvgueniGustavus DirkHoffmeister HansAtmaca AkinJäger Elke - An individual's host genetics influence its susceptibility to both COVID-19 and coronary artery disease (CAD). We analyzed large-scale GWAS datasets encompassing 7.7 million SNPs to identify shared genetic architecture between the two diseases. We identified 24 pleiotropic risk loci for both COVID-19 and CAD, with three loci (1p31.1, 8p21.3, and 18q11.2) showing strong evidence for a single shared causal variant. Loci in the 8p21.3 and 18q11.2 regions showed a bidirectional causal association: COVID-19 to CAD or vice versa, while the 1p31.1 locus only showed a CAD to COVID-19 unilateral casual association in a Mendelian randomization analysis (GSMR). A fine mapping analysis of the three loci identified three lead pleiotropic variants (rs7515509, rs8192330, and rs4800403). The variant rs7515509 was spatially associated with , and ; rs8192330 with , and several other genes; and rs4800403 with and . Transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from COVID-19 patients validated proxitropic variants (rs8192330 and rs4800403) with distinct expression signatures and prioritized and as the likely causal genes. Overexpression of has been linked to the heme metabolism hallmark, disrupted iron distribution in COVID-19 patients with comorbid CAD, and subsequent stress erythropoiesis, oxidative stress, immunological dysfunction, and altered wound healing, while a lower expression of has been observed in the cytoplasmic translation and regulation of mRNA metabolism. In conclusion, we identified shared genetic components for COVID-19 and CAD and prioritized and as the likely causal genes for the observed shared genetic risk. COVID-19 may act as an acute stressor that unmask or accelerates underlying CAD. - Source: PubMed
Publication date: 2026/05/05
Ali Muhammad SarfrazHaider WaseemAziz SanaMohammad AnwaruddinManichaikul AniShi Weibin - Nonsteroidal anti-inflammatory drugs (NSAIDs) can exacerbate urticaria and/or angioedema in up to 30% of patients with chronic urticaria (CU), representing a distinct subtype characterized by heightened inflammation and leukotriene-driven pathophysiology. MicroRNAs (miRNAs) are post-transcriptional regulators that modulate immune and inflammatory responses. This study aimed to identify differentially expressed miRNAs (DEMs) according to NSAID hypersensitivity status and to elucidate their molecular networks in CU. Serum miRNA profiles were analyzed in 14 NSAID-exacerbated CU (NECU) and 16 NSAID-tolerant CU (NTCU) patients using an Affymetrix GeneChip miRNA 4.0 Array. DEMs were identified (fold difference > 1.5, < 0.05), and validated targets were retrieved from the multiMiR database for network construction and Gene Ontology enrichment analyses. NECU patients exhibited a higher frequency of angioedema and systemic corticosteroid use than NTCU patients. Eight DEMs were identified, including upregulated miR-5001-5p, miR-4270, and miR-6869-5p, and downregulated miR-6511b-5p, miR-2277-5p, and miR-378h in NECU. Network integration revealed , , and as central clusters, implicating dysregulation of mRNA decay and inflammatory signaling pathways. Reduced miR-6511b-5p expression may derepress , enhancing chromatin accessibility for inflammatory and leukotriene-synthetic genes. Distinct miRNA signatures differentiate NECU from NTCU, implying a miR-5001-5p/miR-6511b-5p-mRNA decay axis that links impaired post-transcriptional regulation with leukotriene-driven inflammation in CU. These findings highlight candidate miRNAs as potential biomarkers for disease endotyping and therapeutic stratification. - Source: PubMed
Publication date: 2026/01/16
Ye Young-MinNoh Jin YoungKim Seung HoYoon JiwonMoon Da-HyeChoi BoyounPark Se-MinPark Kun-WooKim JungmoWoo Hyun Goo - The general transcription factor TFIIE is believed to be universally required for RNA polymerase II (Pol II)-mediated transcription initiation. However, our biochemical assays and ENCODE ChIP-seq data suggest a more gene-selective role. Using Mediator-depleted HeLa nuclear extracts, we show that TFIIE can be less critical for transcription in the presence of endogenous nuclear components, whereas purified systems of GTFs, Pol II, and Mediator reveal TFIIE to be required for transcription. This conditional requirement led us to hypothesize that TFIIE acts only at a subset of promoters in vivo. Analysis of ENCODE datasets from K562 cells identified transcription start sites (TSS) classified as TFIIE-only by peak calling, lacking annotated TBP, ZZZ3, or MED1, alongside promoters co-bound by all. When we inspected the bigWig signal tracks, they revealed additional co-enrichment not captured by peak calls, suggesting that TFIIE-only sites reflect classification thresholds and not strict exclusivity. Heatmap analyses of TFIIE-bound promoters revealed selective co-enrichment with TBP, ZZZ3 and weaker enrichment with MED1, supporting a non-canonical pre-initiation complex configuration. Gene ontology analysis of these TFIIE-enriched promoters shows strong correlation to chromatin-related processes, suggesting that TFIIE coordinates transcription initiation with chromatin organization and genome stability. - Source: PubMed
Publication date: 2026/01/20
Cevher Murat AWijerathne Pasindu NYozgat YaseminCevher SevdaIto KeiichiCihan AliZaynullina GulnaraPan ShiQiKarlic Serena - Extracellular vesicles (EVs) mediate intercellular communication by transferring microRNAs (miRNAs) that regulate gene expression post-transcriptionally. EVs derived from mesenchymal stem/stromal cells (MSCs) have been widely investigated, and many studies have reported the presence of miRNAs within these vesicles. However, a comprehensive analysis comparing datasets to identify miRNA functional patterns has not yet been conducted. To address this gap, we compiled and analyzed published data on miRNAs in MSCs-derived EVs to uncover common features and explore regulatory roles. A literature search was performed to identify in vitro studies involving human MSCs that provided detailed methodologies for EVs concentration and miRNA characterization. Selected miRNA datasets were used for downstream bioinformatic analyses. Validated miRNA-target gene interactions were retrieved using MultiMiR R package. Functional enrichment analyses were performed using Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways to investigate potential biological roles of the identified genes. We curated 461 studies reporting miRNAs in MSCs-derived EVs. The most studied cells were adipose-derived (ADSCs), bone marrow-derived (BMMSCs), and umbilical cord-derived MSCs (UCMSCs), with BMMSCs contributing the highest number of unique miRNAs. hsa-miR-21-5p was the most frequently reported miRNA. For ADSCs, BMMSCs, and UCMSCs, the most frequently targeted genes were ZZZ3, ZZZ3, and PTEN, respectively. Notably, ZZZ3, a chromatin regulator, was prominent in all three cells. GO analysis revealed biological process enrichment in axonogenesis, while KEGG analysis highlighted significant involvement of neutrophil extracellular trap formation and aminoacyl-tRNA biosynthesis. This study provides an integration of miRNA data from human MSCs-derived extracellular vesicles. - Source: PubMed
Publication date: 2025/12/18
da Nóbrega Thaynan EscariãoFerreira de Souza Sobrinho Hellenda Silva Menezes CamilaFogalli Giovani Bressande Souza Ana PaulaEsposito Douglas VictorinoRodrigues Larissa LopesHu HaiyanMarques Marcelo Rocha