ZNF646 antibody - N-terminal region (ARP33712_P050)
- Known as:
- ZNF646 (anti-) - N-terminal region (ARP33712_P050)
- Catalog number:
- arp33712_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF646 antibody - N-terminal region (ARP33712_P050)
Related genes to: ZNF646 antibody - N-terminal region (ARP33712_P050)
- Gene:
- ZNF646 NIH gene
- Name:
- zinc finger protein 646
- Previous symbol:
- -
- Synonyms:
- KIAA0296
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-08
- Date modifiied:
- 2015-07-14
Related products to: ZNF646 antibody - N-terminal region (ARP33712_P050)
Related articles to: ZNF646 antibody - N-terminal region (ARP33712_P050)
- Dermatophytosis is a fungal infection affecting keratinized tissues such as skin, nails, and hair, presenting as red and itchy patches, nail thickening, or hair loss. It affects around 20% of the global population but the genetic architecture remains poorly understood. We performed a genome-wide association meta-analysis of over 250,000 cases and 1.37 million controls from FinnGen, Estonian Biobank, UK Biobank, and the Million Veteran Program and identified 30 genome-wide significant loci, including seven missense variants and two loci in high linkage disequilibrium with missense variants. Top associations were near ZNF646, HLA-DQB1, FLG, FTO, SLURP2, and KRT77. Additionally, dermatophytosis subtype analyses revealed 44 signals. Our results highlight the role of disrupted keratin biology, skin barrier defects, immune dysfunction, and obesity in dermatophytosis risk. We also observed genetic overlap with other skin conditions and obesity-related traits, providing insights into disease mechanisms and potential targets for prevention and treatment. - Source: PubMed
Publication date: 2026/03/06
Haapaniemi HeleEghtedarian ReyhaneTervi AnniinaValliere Jesse Abner ErikOllila Hanna M - Genome-wide association studies (GWAS) have identified numerous body mass index (BMI) loci. However, most underlying mechanisms from risk locus to BMI remain unknown. Leveraging omics data through integrative analyses could provide more comprehensive views of biological pathways on BMI. - Source: PubMed
Publication date: 2025/09/26
Xu HanfeiGupta ShreyashDinsmore IanKollu AbbeyCawley Anne MarieAnwar Mohammad YChen Hung-HsinPetty Lauren ESeshadri SudhaGraff MisaBelow Jennifer EBrody Jennifer AChittoor GeethaFisher-Hoch Susan PHeard-Costa Nancy LLevy DanielLin HonghuangLoos Ruth J FMccormick Joseph BRotter Jerome IMirshahi ToorajStill Christopher DDestefano AnitaCupples L AdrienneMohlke Karen LNorth Kari EJustice Anne ELiu Ching-Ti - Metabolic syndrome and Parkinson's disease have common pathophysiological denominators. This study aimed to investigate how metabolic syndrome contributes to Parkinson's disease progression, as well as the genetic traits shared by PD and MetS. Four hundred and twenty-three newly diagnosed drug-naïve PD patients were analyzed from the Parkinson's Progression Markers Initiative (PPMI) database. We compared longitudinal changes in the total and subscale scores of the Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) between PD patients with and without metabolic syndrome over a five-year follow-up. We assessed the frequency of PD-associated genetic variants in both groups. At baseline, Parkinson's patients with MetS were typically men ( < 0.01) and older ( = 0.04), with a higher Hoehn and Yahr score ( = 0.01) compared with their counterparts without MetS. They showed higher Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) total scores at baseline and in follow-up years 2, 3, 4, and 5 (all -values < 0.05) as analyzed by the Generalized Estimating Equation model. These differences were primarily driven by elevated motor scores (MDS-UPDRS Part III) ( < 0.01). MetS was associated with a higher frequency of the ZNF646.KAT8.BCKDK_rs14235 variant and a lower frequency of the NUCKS1_rs823118 and CTSB_rs1293298 variants. PD patients with MetS had worse motor symptomatology. Both conditions appear to share genetic susceptibility, involving genes related to lipid metabolism (BCKDK), autophagy and inflammation (CTSB), and chromatin regulation (NUCKS1). - Source: PubMed
Publication date: 2025/06/30
Udovin LucasBordet SofíaBarbar HannyOtero-Losada MatildePérez-Lloret SantiagoCapani Francisco - Cerebral small vessel disease (SVD) is known to increase the risk of epilepsy, but the causal relationship between the two remains unclear. This study utilizes Mendelian Randomization (MR) to assess the genetic link between SVD and epilepsy, incorporating additional analyses including colocalization, gene-set, and pathway analysis to provide further evidence for shared mechanisms. We performed a two-sample MR study using 13 SNPs strongly associated with SVD as instrumental variables to assess their causal relationship with epilepsy. We also conducted colocalization analysis to identify shared genetic variants between SVD and epilepsy, gene-set enrichment analysis to explore common biological pathways, and protein-protein interaction (PPI) network analysis to investigate the molecular mechanisms. The MR analysis revealed a significant causal effect of SVD on epilepsy, with an odds ratio (OR) of 1.29 (95% CI: 1.09-1.53, P < 0.001). Colocalization analysis identified three genomic regions (chr1:100-600 kb, chr3:200-700 kb, and chr5:50-500 kb) with evidence of shared genetic variants. Pathway analysis highlighted endothelial cell signaling, blood-brain barrier function, and neuroinflammatory responses as enriched pathways, linking vascular health to neuronal excitability. The PPI network revealed key proteins involved in both vascular and neuronal processes, including ZNF646, PLEKHG1, and NOTCH3, further supporting shared mechanisms. This study provides strong genetic evidence for an association between SVD and epilepsy, with new insights from colocalization, gene-set, and pathway analyses while recognizing the limitations of Mendelian Randomization in establishing temporal causality. The findings suggest that genetic variants affecting vascular health, neuroinflammation, and blood-brain barrier integrity may contribute to both SVD and the risk of epilepsy. These results strengthen the understanding of the shared biological mechanisms underlying these two conditions and highlight SVD as an important risk factor for epilepsy. - Source: PubMed
Publication date: 2025/02/15
Xu QiwuTan GuoxiangZhao YongDing TingHu KeLing Chen - The current level of knowledge on transcriptome responses triggered by (CS) extract in porcine peripheral blood mononuclear cells (PBMCs) after porcine reproductive and respiratory syndrome virus (PRRSV) infection is limited. Therefore, in the present study, we aimed to detect significant genes and pathways involved in CS extract supplementation responsiveness of PBMCs after PRRSV infection. RNA sequencing was conducted on PBMCs, which were isolated from six weaned piglets. The resultant transcriptional responses were examined by mRNA sequencing. Differential expression analysis identified 263 and 274 differentially expressed genes (DEGs) between the PRRSV and CTRL groups, and the PRRSV+CS and CTRL groups, respectively. Among these, and emerged as the most promising candidate genes, potentially influencing the interaction between PRRSV-infected PBMCs and CS extract supplementation through the regulation of gene networks and cellular homeostasis during stress. Two pathways were detected to be associated with CS extract supplementation responsiveness: the cellular response to stress pathway and the NF-kB signaling pathway. Consequently, our study reveals a novel mechanism underlying cellular stress response and the NF-κB signaling pathway in PRRSV-infected PBMCs, and identifies a potential application of CS extract for activating the NF-κB signaling pathway. In conclusion, by supplementing CS extract in PBMC cells infected with PRRSV, we found that CS extract modulates PRRSV infection by inducing cellular stress, which is regulated by the NF-κB signaling pathway. This induced stress creates an adverse environment for PRRSV survival. This study contributes to a deeper understanding of the therapeutic targets and pathogenesis of PRRSV infection. Importantly, our results demonstrate that CS extract has the potential to be a candidate for modulating PRRSV infection. - Source: PubMed
Publication date: 2024/11/15
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