Ask about this productRelated genes to: ZC3H14 Blocking Peptide
- Gene:
- ZC3H14 NIH gene
- Name:
- zinc finger CCCH-type containing 14
- Previous symbol:
- -
- Synonyms:
- FLJ11806, UKp68, NY-REN-37
- Chromosome:
- 14q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-05-15
- Date modifiied:
- 2014-11-19
Related products to: ZC3H14 Blocking Peptide
Related articles to: ZC3H14 Blocking Peptide
- Metastatic melanoma is an aggressive, heterogeneous cancer with early spread and poor prognosis. Transcriptomic analysis identifies potential therapeutic targets. In silico analysis of the GEO dataset GSE7553 compared primary vs metastatic melanoma using differential expression, enrichment (GO/KEGG/Reactome), PPI network construction, and hub-gene prioritization. Candidates were validated through survival analysis, mutation-associated analyses, and virtual screening using molecular docking with FDA-approved compounds. Transcriptomic results show divergence between primary and metastatic melanoma samples, with principal component analysis supporting clear group separation. In a total of 54,675 probe-level entries, 4868 were classified as upregulated and 10,269 as downregulated, indicating a predominance of downregulated transcriptional events in metastatic melanoma. Prioritized upregulated genes included CUL5, ZC3H14, SON, BRCC3, and H3-3B, whereas notable downregulated genes included ZNF709, CD84, STARD8, EPOR, and HAVCR2. The high-confidence PPI network comprised 625 nodes and 2661 edges, with a significant enrichment score. Enrichment analysis implicated immune/adhesion and translation pathways (e.g., Rap1, focal adhesion, T-cell activation). Survival: CUL5 (HR = 0.26) and ZC3H14 (HR = 0.60) are protective, while SON (HR = 2.4) is adverse. Mutation-linked transcriptomic analysis identified 10 significantly altered genes, including downregulated SNHG18 and upregulated LPCAT2. Virtual screening results show repurposable compounds, with Floxacrine showing strong predicted affinity for CUL5 and Dihydroergocristine showing favorable interaction with LPCAT2/ZC3H14-related targets. In silico docking results further supported CUL5-Floxacrine and LPCAT2-Dihydroergocristine as notable candidate interactions. Results show key transcriptomic drivers and targets (CUL5, ZC3H14, SON, BRCC3, LPCAT2) in metastatic melanoma. Results highlight a useful hypothesis-generating framework for biomarker prioritization and drug repurposing in melanoma. However, independent cohort validation and experimental confirmation are required before clinical translation. - Source: PubMed
Publication date: 2026/05/02
Majeed Khulood AyadMajeed Raghad AyadIbrahim Taisir KhalilKhan Najeeb Ullah - Heterotaxy (HTX) is a congenital disorder characterized by abnormal left-right organ placement, often leading to severe congenital heart disease (CHD). Despite advances in sequencing, many CHD and HTX-associated genes remain functionally unvalidated, hindering effective clinical diagnosis and management. Here, we leveraged a high-throughput CRISPR-Cas9 screening approach in the Xenopus model to rapidly evaluate candidate genes identified from whole-exome sequencing of human CHD patients. Our screen identified Filamin B (FLNB), an actin-binding protein previously linked to skeletal disorders but not to ciliopathies or CHD. We identified 5 probands with CHD and HTX, 3 with recessive and 2 with damaging heterozygous variants in FLNB. Disrupting flnb in Xenopus reproduced key features of the human HTX phenotype, including defects in cardiac development and impaired motile cilia function. Rescue experiments confirmed the functional conservation of human FLNB, directly implicating actin cytoskeletal disruption in ciliogenesis and left-right patterning defects. Our results provide crucial evidence linking human FLNB dysfunction to ciliopathies and CHD and HTX. - Source: PubMed
Publication date: 2026/02/10
Arrigo AngeloRao VenkatramananRatan AakroshKulkarni Saurabh S - Heterotaxy (HTX) syndrome is a congenital disorder characterized by abnormal left-right organ placement, often leading to severe congenital heart defects (CHD). Despite advances in sequencing, many CHD/HTX-associated genes remain functionally unvalidated, hindering effective clinical diagnosis and management. Here, we leveraged a high-throughput CRISPR/Cas9 screening approach in the model to rapidly evaluate candidate genes identified from whole-exome sequencing of human CHD patients. Our screen identified Filamin B (FLNB), an actin-binding protein previously linked to skeletal disorders but not to ciliopathies or CHD. We identified 5 probands with CHD/HTX, 3 with recessive, and 2 with damaging heterozygous mutations in FLNB. Disrupting FLNB in reproduced key features of the human HTX phenotype, including defects in cardiac development and impaired motile cilia function. Rescue experiments confirmed the functional conservation of human FLNB, directly implicating actin cytoskeletal disruption in ciliogenesis and left-right patterning defects. Our results provide crucial evidence linking human FLNB dysfunction to ciliopathies and CHD/HTX. - Source: PubMed
Publication date: 2025/10/15
Arrigo AngeloRao VenkatramanRatan AakroshKulkarni Saurabh S - Polyadenylation of mRNA is a key step in post-transcriptional regulation. In this issue of , Gabs and colleagues (doi:10.1101/gad.352912.125) provide evidence for a novel, kinetically driven mechanism that dictates the length of poly(A) tails added to mRNAs in budding yeast. The investigators introduce the concept of Nab2, a zinc finger poly(A) RNA binding protein, as a "kinetic ruler," which functions through dynamic competition with the cleavage and polyadenylation complex (CPAC) to define the length of poly(A) tails. - Source: PubMed
Publication date: 2025/11/03
Corbett Anita H - Diabetes is considered to be a risk factor for colon cancer (CC), and CC patients with diabetes tend to have a worse prognosis. However, the underlying mechanism of this condition remains unclear. This study aims to elucidate the relationship between diabetes and CC further, and to find effective therapeutic targets. - Source: PubMed
Publication date: 2025/08/24
Yao MingWang RongzhongCui RonghaiLou FanChen Zelian