Ask about this productRelated genes to: ZDHHC13 Blocking Peptide
- Gene:
- ZDHHC13 NIH gene
- Name:
- zinc finger DHHC-type containing 13
- Previous symbol:
- -
- Synonyms:
- FLJ10852, FLJ10941, HIP14L
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-07
- Date modifiied:
- 2016-02-15
Related products to: ZDHHC13 Blocking Peptide
Related articles to: ZDHHC13 Blocking Peptide
- Cardiac injury from lipid overload features cardiomyocyte death, myocardial remodeling, and reduced contractile function. Although L-menthol has reported cardioprotective effects, its mechanisms are poorly defined. We therefore examined the role of transient receptor potential melastatin 8 (TRPM8) in lipid overload-induced cardiac dysfunction and tested whether L-menthol acts via TRPM8. After 12 weeks of high-fat diet, mouse ventricular myocytes showed a marked reduction in TRPM8 protein expression. In vitro, L-menthol reduced cardiomyocyte injury caused by lipid overload, and in vivo it mitigated cardiac injury in high-fat diet fed male mice. These protective effects were largely abolished by TRPM8 knockdown, indicating a TRPM8-dependent mechanism. Mechanistic studies indicate that L-menthol preserves mitochondrial Ca homeostasis via a TRPM8/GRP75/VDAC1 associated pathway, which limits mitochondrial dysfunction and apoptosis during lipid overload. We also found that lipid overload decreased TRPM8 S-palmitoylation at the C707 regulatory site and reduced TRPM8 protein stability. Downregulation of zDHHC13 may contribute to this loss of S-palmitoylation, whereas L-menthol helped maintain TRPM8 S-palmitoylation and protein expression. Together, these results support a TRPM8-dependent protective effect of L-menthol against lipid overload-induced cardiac injury and suggest that TRPM8-related signaling may represent a potential therapeutic target. - Source: PubMed
Publication date: 2026/05/08
Sun XiangDing QiruiZhou YuyanHuang SichaoLiu XinyuSong YingYi ZeshuaiMa LuTeng WeiLi XiaoxuSun BinLi Baoxin - Intracranial aneurysms (IAs) can cause life-threatening subarachnoid hemorrhage upon rupture, yet their molecular mechanisms remain poorly understood. Proteins encoded by the ZDHHC genes mediate protein palmitoylation and are involved in brain injury processes, but their relationship with IA rupture is unclear. - Source: PubMed
Publication date: 2026/02/19
Zhang WanjingLiu LuHou YajunWang Weiqi - Autism spectrum disorder (ASD) has a complex genetic etiology, with limited data from Indian populations. This study delineates the genetic architecture of ASD in Indian children using whole exome sequencing (WES) and exploratory genetic association studies (GASs). - Source: PubMed
Publication date: 2026/01/21
Naushad Shaik MohammadEsdhan Basha ShaikKanaka Durga Devi Yadam ReddyPalanikumar PalanichamyKonanki Ramesh - The intratumor microenvironment shapes the metastatic potential of cancer cells and their susceptibility to any immune response. Yet, the nature of the signals within the microenvironment that control anticancer immunity and how they are regulated is poorly understood. Here, using melanoma as a model, we investigate the involvement in metastatic dissemination and the immune-modulatory microenvironment of Protein S-Acyl Transferases as an underexplored class of potential therapeutic targets. We find that ZDHHC13 suppresses metastatic dissemination by palmitoylation of CTNND1, leading to stabilization of E-cadherin. Importantly, ZDHHC13 also reshapes the tumor immune microenvironment by suppressing lysophosphatidylcholine (LPC) synthesis in melanoma cells, leading to inhibition of M2-like tumor-associated macrophages that we show degrade E-cadherin via MMP12 expression. Consequently, ZDHHC13 activity suppresses tumor growth and metastasis in immunocompetent mice. Our study highlights the therapeutic potential of targeting the ZDHHC13-E-cadherin axis and its downstream metabolic and immune-modulatory mechanisms, offering additional strategies to inhibit melanoma progression and metastasis. - Source: PubMed
Publication date: 2025/09/30
Li HongjinLyu JiankeSun YuYin ChengqianLi YuewenChen WeiqiangFoo Suan-SinWu XianfangGoding Colin RChen Shuyang - This work examined the causal link between palmitoylation-related genes and Parkinson's disease (PD) by Mendelian randomization (MR). We conducted two-sample Mendelian randomization utilizing genome-wide association study (GWAS) summary statistics. Expression quantitative trait loci (eQTL) data for palmitoylation genes were sourced from eQTLGen, whilst PD data were derived from the GWAS Catalogue (15,056 cases, 12,637 controls) and FinnGen (4,681 cases, 407,500 controls). Instrumental variables (p < 5 × 10⁻⁶, r < 0.1) were examined using inverse-variance weighted (IVW) regression, along with weighted median, MR-Egger, and Summary-data-based MR (SMR) methods. Sensitivity analyses evaluated pleiotropy and resilience. The IVW analysis revealed significant correlations with Parkinson's disease for ZDHHC14 (OR = 1.09, P = 0.037), ZDHHC17 (OR = 1.18, P = 0.002), ZDHHC2 (OR = 1.16, P = 0.039), ZDHHC20 (OR = 0.82, P = 0.019), and ZDHHC8 (OR = 1.24, P = 0.022). SMR validation corroborated solely ZDHHC8 (OR = 1.35, P = 0.040). Replication in FinnGen corroborated ZDHHC1, ZDHHC13, ZDHHC17, and ZDHHC8. No heterogeneity or pleiotropy was observed (P > 0.05). ZDHHC8 has a strong causative relationship with PD, suggesting that palmitoylation dysregulation plays a role in disease etiology. These findings underscore synaptic dysfunction as a viable therapeutic target. - Source: PubMed
Publication date: 2025/10/21
Qiu JinYang JialiZhu RuisenXian DeHaiYang Kaiwen