Ask about this productRelated genes to: ZNF415 antibody
- Gene:
- ZNF415 NIH gene
- Name:
- zinc finger protein 415
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-20
- Date modifiied:
- 2015-09-29
Related products to: ZNF415 antibody
Related articles to: ZNF415 antibody
- Stillbirth (SB) in dairy cattle is both an animal welfare and an economic issue. The reasons for SB and how traits like gestation length (GL) influence it are part of ongoing research. Utilizing imputed high-density (HD) and whole-genome sequencing (WGS) genotypes from 34,497 German Holstein cows, this study aimed to identify local genetic correlation in trait associated genomic regions for SB and GL. For this, regional heritability mapping (RHM) was conducted, alongside analyses of global and local genetic correlation. In the downstream analysis, regions showing significant local genetic correlations within significant RHM windows were searched for candidate genes. RHM of direct effects on GL resulted in 2 significant regions on BTA18 and 19 in first (GL_d1) and second parity (GL_d2). One region on BTA9 was significant for the maternal effect on SB. Significant global genetic correlations were confined to a low negative correlation of -0.17 (SE = 0.04) between SB direct (SBd) and GL_d1. Their local genetic correlations were negative on BTA18 and positive on BTA19, with ZNF415 and SLC43A2 as candidate genes. The gene ontology enrichment analysis for SBd and GL_d1 identified biologically relevant pathways, with the largest cluster related to the transport of organic acids and amino acids. Overall, the study achieved insights into the complex genetic architecture of SB and its interaction with GL. Candidate genes of still unknown function should be considered by future research to further strengthen the understanding of trait interactions. - Source: PubMed
Publication date: 2026/04/09
Zölch MaximilianHaas Valentin PKeßler FranziskaKrižanac Ana-MarijaReimer ChristianSchmidtmann ChristinAlkhoder HatemTetens JensBennewitz Jörn - Alzheimer's disease (AD) is a complex neurodegenerative disorder driven by multilayered molecular and cellular mechanisms that cannot be fully elucidated through single-omics approaches. Consequently, large-scale multi-omics integration-encompassing transcriptomics, epigenomics (e.g., methylation), and genetic association studies (GWAS/eQTL/mQTL)-has uncovered critical genetic and epigenetic networks underlying disease risk and progression.Based on these integrative insights, this review emphasized several genes-including KLHL21, SCN2B, ZNF415, and PITRM1-as potential contributors to AD pathogenesis. Notably, single-cell and spatial transcriptomics analyses revealed specific enrichment of these genes in astrocytes, underscoring the pivotal role of this cell type in Aβ clearance, tau propagation, and neuroinflammation. Exercise interventions were shown to selectively modulate the expression of these genes, providing molecular support for the preventive and therapeutic potential of non-pharmacological lifestyle strategies. Drug repurposing analyses using DrugBank have identified promising therapeutic candidates, including FDA-approved agents (e.g., valproic acid, raloxifene, and clomipramine) and naturally derived compounds (e.g., quercetin and fisetin), which may modulate key AD-related pathways. Furthermore, emerging evidence of miRNA-gene regulatory networks suggested an additional layer of post-transcriptional control that may regulate responses to pathological stimuli. Collectively, these integrative insights advocated for a multidimensional precision medicine framework that spans genetic, cellular,network, and lifestyle levels of regulation. This shift from single-target therapeutics to an integrated "gene-cell-network-lifestyle" paradigm open new theoretical and translational avenues for delaying or mitigating AD progression. - Source: PubMed
Publication date: 2025/11/19
Su LiningWang Yanbing - The most promising treatment options for severe uncontrolled asthma (SUA) have emerged in recent years with the development of monoclonal antibodies for blocking selective targets responsible for the underlying inflammation, such as mepolizumab and benralizumab. However, there is variability in treatment response that is not fully controlled. The variability of the response to mepolizumab and benralizumab could be influenced by single-nucleotide polymorphisms (SNPs), and it would be useful to detect these and use them as predictive biomarkers of response. We conducted a retrospective observational cohort study of 72 Caucasian patients recruited from a tertiary hospital with severe uncontrolled eosinophilic asthma treated with mepolizumab and benralizumab. Polymorphisms in the (rs4143832, rs17690122), (rs11739623, rs4705959), (rs1420101, rs17026974, rs1921622), (rs4857855), (rs12619285), (rs1801274), (rs3219018, rs1050501), (rs10127939, rs396991), (rs2251746, rs2427837), (rs1441586, rs573790, rs569108), and (rs1054485) genes were analyzed by real-time polymerase chain reaction (PCR) using Taqman probes. The response was analyzed after 12 months of treatment. In patients under mepolizumab treatment, a treatment response defined as a reduction in exacerbations was associated with rs1054485-T ( = 0.042; OR = 5.33; 95% CI = 1.06-30.02), treatment response defined as a reduction in oral corticosteroids use was associated with the number of exacerbations in the previous year ( = 0.029; OR = 3.89; 95% CI = 1.24-14.92), and treatment response defined as improvement in lung function was associated with the age at the beginning of biological therapy ( = 0.002; OR = 1.10; 95% CI = 1.04-1.18), rs569108-AA ( < 0.001; OR = 171.06; 95% CI = 12.94-6264.11), and rs2427837-A ( = 0.021; OR = 8.61; 95% CI = 1.71-76.62). On the other hand, in patients under benralizumab treatment, treatment response, defined as a reduction in exacerbations, was associated with rs1054485-T ( = 0.073; OR = 1.3 × 10; 95% CI = 1.8 × 10-NA), rs569108-AA ( = 0.050; OR = 11.51; 95% CI = 1.19-269.78), allergies ( = 0.045; OR = 4.02; 95% CI = 1.05-16.74), and sex ( = 0.028; OR = 4.78; 95% CI = 1.22-20.63); and treatment response defined as improvement in lung function was associated with polyposis ( = 0.027; OR = 9.16; 95% CI = 1.58-91.4), rs12619285-AA ( = 0.019; OR = 9.1; 95% CI = 1.7-75.78), rs4143832-T ( = 0.017; OR = 11.1; 95% CI = 1.9-112.17), and rs1441586-C ( = 0.045; OR = 7.81; 95% CI = 1.16-73.45). The results of this study show the potential influence of the studied polymorphisms on the response to mepolizumab and benralizumab and the clinical benefit that could be obtained by defining predictive biomarkers of treatment response. - Source: PubMed
Publication date: 2024/07/26
Rojo-Tolosa SusanaSánchez-Martínez José AntonioCaballero-Vázquez AlbertoPineda-Lancheros Laura ElenaGonzález-Gutiérrez María VictoriaPérez-Ramírez CristinaJiménez-Morales AlbertoMorales-García Concepción - Patients with late-stage mild cognitive impairment (LMCI) have a higher risk of progression to Alzheimer's disease (AD) than those with early-stage mild cognitive impairment (EMCI). However, previous studies have often pooled EMCI and LMCI patients into a single MCI group, with limited independent investigation into the pathogenesis of LMCI. In this study, we employed whole-genome methylation association analysis to determine the differences in peripheral blood methylation profiles between 663 cognitive aging (CN) and 554 LMCI patients. Our results revealed 2,333 differentially methylated probes (DMPs) and 85 differentially methylated regions (DMRs) specific to LMCI. The top hit methylation sites or regions were associated with genes such as SNED1, histone deacetylases coding gene HDACs, and HOX and ZNF gene family. The DNA methylations upregulated the expression of HDAC4, HDAC8, and HOX family genes HOXC5 and HOXC9, but they downregulated the expression of SNED1, ADCYAP1, and ZNF family genes ZNF415 and ZNF502. Gene Ontology (GO) and KEGG analysis showed that the genes associated with these methylation sites were predominantly related to the processes of addiction disorders, neurotransmission, and neurogenesis. Out of the 554 LMCI patients included in this study, 358 subjects (65%) had progressed to AD. Further association analysis between the LMCI subjects with a stable course (sLMCI) and those who progressed to AD (pLMCI) indicated that the methylation signal intensities of HDAC6, ZNF502, HOXC5, HOXC6, and HOXD8 were associated with increased susceptibility to AD. Protective effects against progression to AD were noticed when the methylation of SNED1 and ZNF727 appeared in LMCI patients. Our findings highlight a substantial number of LMCI-specific methylated biomarkers that differ from those identified in previous MCI case-control studies. These biomarkers have the potential to contribute to a better understanding of the pathogenesis of LMCI. - Source: PubMed
Publication date: 2024/01/16
Zhang YiShen Shasha - Sarcopenia is a common chronic disease characterized by age-related decline in skeletal muscle mass and function, and the lack of diagnostic biomarkers makes community-based screening problematic. - Source: PubMed
Publication date: 2022/09/13
Lin ShangjinLing MingChen CongCai XiaoxiYang FengjianFan Yongqian