ZDHHC18 Antibody
- Known as:
- ZDHHC18 Antibody
- Catalog number:
- GWB-MP232G
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- ZDHHC18 Antibody
Related genes to: ZDHHC18 Antibody
- Gene:
- ZDHHC18 NIH gene
- Name:
- zinc finger DHHC-type containing 18
- Previous symbol:
- -
- Synonyms:
- DKFZp667O2416
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-21
- Date modifiied:
- 2016-02-15
Related products to: ZDHHC18 Antibody
Related articles to: ZDHHC18 Antibody
- Palmitoylation in neurodisorders is increasingly recognized, but the specific molecular mechanisms and metabolic networks underlying epileptic pathogenesis remain poorly understood. Using a multi-omics integrative strategy, this work intended to systematically examine the contribution of palmitoylation-related genes to epilepsy. - Source: PubMed
Publication date: 2026/03/18
Fu JiaZhao JingSi YaoSun LinlinSun LinaFan YuweiZhang ChaoYao Lifen - Meniere's disease (MD) is a heterogeneous, rare inner ear disorder characterized by recurrent vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness. Its molecular mechanisms remain unclear due to significant clinical and immunological heterogeneity. In this study, we integrated multi‑omics genetic data to systematically screen for palmitoylation regulatory genes associated with MD risk. We first intersected 31 core palmitoylation genes with blood cis‑eQTL datasets to identify candidate expression‑related genes, then performed two‑sample Mendelian randomization (MR) to examine their genetic correlation with MD. Summary‑data‑based MR (SMR) using two independent peripheral blood eQTL cohorts (eQTLGen and GTEx) was further applied to validate robust candidate genes. Two‑sample inverse‑variance weighted (IVW) MR revealed nominally significant associations between PPT2, ZDHHC18, ZDHHC5 and MD risk. Independent SMR validation confirmed that peripheral ZDHHC5 expression was significantly correlated with MD (eQTLGen: PSMR = 0.023; GTEx: PSMR = 0.006), and a non‑significant HEIDI test ruled out strong linkage disequilibrium confounding. We further explored potential immune mediators using a two‑step MR screening framework covering 731 peripheral immune cell phenotypes. After Benjamini-Hochberg false discovery rate (FDR) correction for all immune traits to control for multiple testing, no immune cell phenotype retained an FDR < 0.05 association with MD; therefore, formal mediation analysis was not conducted. In summary, this MR‑based genetic analysis identifies ZDHHC5 as a gene associated with MD susceptibility. The potential immune regulatory axis involving NKT cells remains speculative and requires validation through large‑scale stratified immune cohort data and functional cellular/animal experiments. No definitive causal or therapeutic conclusions can be drawn from the present genetic statistical evidence alone. - Source: PubMed
Publication date: 2026/08/13
Li RuilongChen Keguang - Hepatocellular carcinoma (HCC) remains a significant global health burden, with high mortality rates due to late diagnosis and limited therapeutic options. Palmitoylation, a reversible post-translational modification, has emerged as a critical regulator of cancer progression, yet its role in HCC remains underexplored. This study aims to investigate the diagnostic and prognostic value of palmitoylation-related genes (acyltransferase and acylthioesterase) in HCC, focusing on their potential as biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/07/28
Gao XiangWang FangzhouQu YuanxuLiu YingaoZheng Yamin - ObjectivesCircadian rhythms regulate human health, and observational studies have linked their disruption to hypertension; however, confounding factors and reverse causality limit causal interpretation. We aimed to evaluate the existing evidence linking circadian gene sets and hypertension using Mendelian randomization.MethodsTwo-sample Mendelian randomization was performed using genome-wide association study summary-level data from non-overlapping European ancestry samples. Genetic variants of 1276 circadian genes () were instrumental variables; the outcome was hypertension genome-wide association study data from the UK Biobank (ieu-b-5144; 463,010 participants). Single nucleotide polymorphisms were selected at <5 × 10 (mean F-statistic: 276.5). Inverse variance weighting was the primary method used. Benjamini-Hochberg false discovery rate correction was applied across all 1276 genes. Sensitivity analyses were performed using heterogeneity testing, Mendelian randomization-Egger regression, Mendelian Randomization Pleiotropy RESidual Sum and Outlier, Steiger directionality testing, and leave-one-out analyses.ResultsMendelian randomization identified 39 nominally significant associations (inverse variance weighting, < 0.05). After false discovery rate correction, four genes reached statistical significance: (odds ratio = 0.988, 95% confidence interval: 0.983-0.993), (odds ratio = 1.009, 95% confidence interval: 1.005-1.014), (odds ratio = 0.990, 95% confidence interval: 0.986-0.995), and (odds ratio = 1.012, 95% confidence interval: 1.007-1.018). The remaining nominal associations did not survive false discovery rate correction and were classified as exploratory. Functional enrichment implicated circadian rhythm, apoptosis, and glycosaminoglycan biosynthesis pathways. Sensitivity analyses did not reveal significant heterogeneity or pleiotropy.ConclusionsThese findings are hypothesis-generating and require experimental validation. , , , and demonstrated statistically significant associations with hypertension risk after false discovery rate correction and should be prioritized for follow-up. Other nominal findings should be interpreted as exploratory. - Source: PubMed
Publication date: 2026/08/11
Wang Lu-JieLeng Yue-QiWang Wei-ZhongSun Jia-Cen - Cardiac hypertrophy, a significant pathological response to various stressors, often culminates in heart failure and necessitates the identification of novel regulatory targets for developing effective therapeutic strategies. In our study, an integrated transcriptomic and proteomic analysis revealed that deubiquitinating enzyme 13 (USP13) was significantly downregulated during cardiac hypertrophy. Subsequent functional experiments confirmed that USP13 overexpression markedly ameliorated transverse aortic constriction-induced cardiac dysfunction and attenuated cardiomyocyte hypertrophy, indicating that USP13 functions as a potential suppressor of this pathological condition. Mechanistic studies demonstrated that USP13 bound to and deubiquitinated sorting nexin 13 (SNX13), thereby stabilizing the SNX13 protein. SNX13 promoted nuclear accumulation of Nrf2, upregulating key ferroptosis-related genes including SLC7A11 and GPX4, thereby attenuating ferroptosis and ameliorating cardiac hypertrophy. Additionally, the m6A reader YTHDF2 was found to bind m6A-modified USP13 mRNA, facilitating its degradation and subsequent reduction in USP13 expression. We also established that the palmitoyltransferase ZDHHC18 enhanced YTHDF2 stability by mediating YTHDF2 S-palmitoylation, specifically at Cys468. This study identifies a functional ZDHHC18/YTHDF2/USP13/SNX13/Nrf2/ferroptosis signaling axis in cardiac hypertrophy, highlighting its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/07/18
Ba LinaWang RuixuanZhao ZhichaoDu YangyangWang RuiWu NanZhang QianhuiSun HongliQi Hanping