Ask about this productRelated genes to: ZDHHC19 Blocking Peptide
- Gene:
- ZDHHC19 NIH gene
- Name:
- zinc finger DHHC-type containing 19
- Previous symbol:
- -
- Synonyms:
- MGC33345
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-21
- Date modifiied:
- 2016-02-15
Related products to: ZDHHC19 Blocking Peptide
Related articles to: ZDHHC19 Blocking Peptide
- Vascular endothelial growth factor A (VEGFA) plays a critical role in the pathogenesis of diabetic macular edema (DME) in patients with type 2 diabetes mellitus (T2DM). Herein, we sought to determine whether palmitoylation modulates the stability and function of VEGFA in the context of DME. - Source: PubMed
Publication date: 2026/07/25
Jiang LiYang Ming-MingLiu Ying-RuiDeng Ting-MingZhang Kun - Anemia is a common complication of tuberculosis (TB), closely associated with impaired host immune function and poor prognosis; however, its impact on the dynamic alterations of erythroid progenitor cells (EPCs) remains largely unexplored. In this study, we integrated and analyzed single-cell transcriptomic data from peripheral blood mononuclear cells (PBMC) of healthy controls, latent tuberculosis (LTB), TB, and disseminated tuberculosis (DTB) cohorts, as well as 18F-FDG-labeled TB lung tissues and adjacent uninvolved regions. At single-cell resolution, we identified ten EPCs clusters within PBMC, among which clusters 2-6 represented DTB-specific subpopulations (EPC_DTB). These EPC_DTB exhibited metabolic reprogramming (including glycolysis, arginine, and lipid metabolism) accompanied by upregulation of IFITM3/JUN and ribosomal genes, consistent with enhanced differentiation. EPC_DTB and EPC_TB interacted with macrophages, dendritic cells, and monocytes through the ANNEXIN and GALECTIN signaling pathways, while these immune cells reciprocally regulated EPCs subsets via the MIF signaling axis. In lung tissues, EPCs (12 clusters) displayed disease-specific characteristics, with clusters 0, 3, and 6 uniquely present in TB lesions. The EPC_High subpopulation within inflammatory foci showed significant upregulation of GZMA, IL32, CCL5, and CHI3L1, whereas EPC_Low communicated with immune cells, epithelial cells, and stromal cells through the MDK-NCL signaling pathway. Moreover, we established an LTB predictive model based on EPC_LTB signature genes in PBMC (GRIK3, S100B, ZDHHC19, and LRRN3). Our study uncovers the heterogeneity of EPCs across different TB stages and tissue compartments, delineates their bidirectional crosstalk with immune cells, and establishes a link among anemia, immune regulation, and EPCs biology, thereby proposing potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/02/16
Zhang HaoCao YanYang LingLiu BowenGuan JingzhiWang Xinjing - Palmitoylation plays a crucial role in the development of cancer, but the causal relationship with oral cancer is still uncertain. The aim of this study was to describe the causal relationship between palmitoylation modified genes and oral cancer, while identifying intermediate factors. Genome-wide association studies of immune cells, oral cancer, and palmitoylation gene expression quantitative trait locus were derived from public databases. In this study, inverse variance weighting was used as the primary analytical method to investigate the causal relationship between exposure and outcome. In addition, this study uses Mendelian randomization (MR) Egger, simple mode, weighted median and weighted mode as supplementary analysis methods. To ensure the reliability of the findings, we further assessed horizontal pleiotropy and heterogeneity, and used the leave-one-out method to assess the stability of the MR results. Finally, mediated analysis was used to elucidate the potential mediated role of immune cell phenotype. Two-sample MR analysis revealed a causal relationship between palmitoylation genes and oral cancer. The results showed that zinc finger DHHC-type containing 19 (odds ratio [OR] = 0.6482, 95% CI: 0.5335-0.7875, P < .001) was negatively correlated with the occurrence of oral cancer. Zinc finger DHHC-type (ZDHHC)2 (OR = 1.6051, 95% CI: 1.3389-1.9242, P < .001) and ZDHHC24 (OR = 1.6077, 95% CI: 1.1588-2.2305, P = .0045) were positively correlated with oral cancer. The results of mediated MR analysis showed that CD28+ CD45RA+ CD8br absolute cell counts positively regulated ZDHHC2 and oral cancer (mediation effect [ME] = 0.0801; mediation proportion [MP] = 16.92%). CD28- CD8br absolute cell counts (ME = 0.0747; MP = 17.23%) and CD25 on IgD- CD38dim (ME = 0.0164; MP = 3.78%) positively modulated ZDHHC19- oral cancer. This study provides evidence supporting a causal relationship between palmitoylation genes and oral cancer, with immune cell phenotypes acting as mediators. Identifying a potential causal relationship between palmitoylation genes and oral cancer reveals its underlying mechanisms and suggests new therapeutic targets. - Source: PubMed
Jiang Zhong-HuiWei Yan-HongXie HangWang Hong-BingHe WeiWang Xin-Juan - BACKGROUND: Polydatin, extracted from Polygonum cuspidatum, has been demonstrated to exert anti-tumor effects and induce apoptosis in several cancers including acute myeloid leukemia (AML). This study explored the potential mechanism of polydatin regulating apoptosis in AML. However, its precise molecular mechanism in AML remains poorly understood. METHODS: Patients with AML or non-malignant hematological disease were recruited for collecting bone marrow samples. In AML cell lines, cell viability and apoptosis were determined with CCK-8 and flow cytometry, respectively. The palmitoylation level of BH3 interacting-domain death agonist (BID) was assessed using Acyl-RAC assay. The interaction between BID and zinc finger DHHC-type palmitoyltransferase 19 (ZDHHC19) was validated by co-immunoprecipitation. Western blot and immunofluorescence were used for measuring protein expression and localization. The role of polydatin in vivo was confirmed by establishing a xenograft model with nude mice, while Ki67 expression and apoptosis in tumors were measured with immunohistochemistry and TUNEL assay. RESULTS: ZDHHC19 and BID palmitoylation were decreased in AML patients and cell lines. In HL-60 and MOLM-13 cells, polydatin treatment reduced cell viability, promoted apoptosis, and increased apoptosis-related proteins including BID, caspase-8, and cytochrome C. BID-cysteine (C)3/15-WT, but not BID-C3/15-Mut, led to increased BID palmitoylation and mitochondrial translocation. Polydatin treatment facilitated BID palmitoylation and apoptosis, when overexpressing BID-C3/15-WT but not BID-C3/15-Mut. The combination and co-localization of ZDHHC19 and BID were confirmed in AML cells. The effects of polydatin on promoting apoptosis and inhibiting tumor growth in vitro and in vivo were antagonized when silencing ZDHHC19. CONCLUSION: This study reveals a novel mechanism by which polydatin promotes apoptosis in AML through ZDHHC19-mediated BID palmitoylation. These findings suggest that polydatin may serve as a promising therapeutic candidate targeting apoptosis in AML. - Source: PubMed
Publication date: 2025/12/06
Zhang WenhuiLiu ZhongwenPei XiaohangHao PeiyuanJiang LingShi MingyueYuan XiaoliZhu Zunmin - S-palmitoylation is a dynamic and reversible post-translational modification that plays crucial roles in cancer progression. Here, we found that the oncogene of metadherin (MTDH) modulates lipid metabolism and ferroptosis by its S-palmitoylation. We demonstrate that MTDH is S-palmitoylated at Cys-75 in the endoplasmic reticulum by ZDHHC1/9 and S-depalmitoylated by APT1. The flexible loop and the α-helix length in the MTDH N-terminus affect its S-palmitoylation level. In addition, metabolomics analysis found that the S-palmitoylated MTDH increases intracellular levels of triglycerides, phosphatidylethanolamines, and phosphatidylcholines. The non-S-palmitoylation form of MTDH-CS enhanced the interaction between MTDH and the ferroptosis enhancer of Acyl-CoA synthetase long-chain family member 4 (ACSL4), thereby reducing ferroptosis sensitivity in breast cancer cells. - Source: PubMed
Publication date: 2025/11/28
Pei ShaojunWang WenFeng TingzeWang QiupingWang YuhanLiu Hong-XuLiang XinmiaoPiao Hai-Long