Ask about this productRelated genes to: ZDHHC16 antibody
- Gene:
- ZDHHC16 NIH gene
- Name:
- zinc finger DHHC-type containing 16
- Previous symbol:
- -
- Synonyms:
- APH2
- Chromosome:
- 10q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-21
- Date modifiied:
- 2016-02-15
Related products to: ZDHHC16 antibody
Related articles to: ZDHHC16 antibody
- Male subfertility is a global health concern, with spermatogenic dysfunction being a critical cause. Abnormally high level of palmitic acid (PA), a main component of dietary saturated fatty acid, has been reported to be implicated in the spermatogenic dysfunction, accompanied with a decrease of inhibin B (INHB). However, the mechanism underlying PA-induced downregulation of INHB, and the specific function of INHB in the spermatogenesis microenvironment, remain unclear. Since PA is the main substrate of palmitoylation, a common post-translational lipid modification, we investigated the role of palmitoylation in INHB synthetic defects and subsequent dyszoospermia induced by PA in this study. - Source: PubMed
Publication date: 2025/12/17
Xiang YijianXu YaoZhang JingZhu MiaoHe ZhaowanyueZang MingMa RujunChen LiLi ZhouDu TianYao LiangyuLiang KuanShen JiamingZhao ShanmeiziJing JunGe XieYao Bing - Autosomal recessive coding variants are well-known causes of rare disorders. We quantified the contribution of these variants to developmental disorders in a large, ancestrally diverse cohort comprising 29,745 trios, of whom 20.4% had genetically inferred non-European ancestries. The estimated fraction of patients attributable to exome-wide autosomal recessive coding variants ranged from ~2-19% across genetically inferred ancestry groups and was significantly correlated with average autozygosity. Established autosomal recessive developmental disorder-associated (ARDD) genes explained 84.0% of the total autosomal recessive coding burden, and 34.4% of the burden in these established genes was explained by variants not already reported as pathogenic in ClinVar. Statistical analyses identified two novel ARDD genes: KBTBD2 and ZDHHC16. This study expands our understanding of the genetic architecture of developmental disorders across diverse genetically inferred ancestry groups and suggests that improving strategies for interpreting missense variants in known ARDD genes may help diagnose more patients than discovering the remaining genes. - Source: PubMed
Publication date: 2024/09/23
Chundru V KartikZhang ZhanchengWalter KlaudiaLindsay Sarah JDanecek PetrEberhardt Ruth YGardner Eugene JMalawsky Daniel SWigdor Emilie MTorene RebeccaRetterer KyleWright Caroline FÓlafsdóttir HildurGuillen Sacoto Maria JAyaz AkifAkbeyaz Ismail HakkiTürkdoğan DilşadAl Balushi Aaisha IbrahimBertoli-Avella AidaBauer PeterSzenker-Ravi EmmanuelleReversade BrunoMcWalter KirstySheridan EamonnFirth Helen VHurles Matthew ESamocha Kaitlin EUstach Vincent DMartin Hilary C - The repair of bone defects caused by periodontal diseases is a difficult challenge in clinical treatment. Dental pulp stem cells (DPSCs) are widely studied for alveolar bone repair. The current investigation aimed to examine the specific mechanisms underlying the role of Zinc finger DHHC-type palmitoyl transferases 16 (ZDHHC16) in the process of osteogenic differentiation (OD) of DPSCs. - Source: PubMed
Publication date: 2024/03/26
Liu WeiYu WenweiZhou LiliLing DanhuaXu YangboHe Fuming - At present, the early diagnosis and treatment of non-small cell lung cancer (NSCLC) is still an urgent problem to be solved worldwide, including in China. The present work investigated the possible protective effect of ZDHHC16 in cell proliferation and metastasis of NSCLC and explored its possible mechanisms. ZDHHC16 expression level in patients with Non-Small-Cell Lung Cancer was up-regulation. ZDHHC16 gene is stabilized by m6A methylation. ZDHHC16 gene reduced ferroptosis of NSCLC by the rehabilitation of the mitochondrial structure. ZDHHC16 promoted CREB expression through the inhibition of CREB Ubiquitination. Confocal microscopy showed that ZDHHC16 reduced the CREB expression of NSCLC. ZDHHC16 up-regulation reduced CREB Ubiquitination, and down-regulation of ZDHHC16 promoted CREB Ubiquitination of NSCLC. CREB Agonists reduced the effects of ZDHHC16 on ferroptosis, not affecting the Warburg effect of NSCLC. CREB inhibitor reduced the effects of si-ZDHHC16 on ferroptosis, not affecting the Warburg effect of NSCLC. METTL3-mediated m6A modification increases ZDHHC16 stability. Our study revealed that the m6A-forming enzyme METTL3 upregulates ZDHHC16 expression in NSCLC patients, leading to the reduction of ferroptosis by inhibiting CREB ubiquitination. - Source: PubMed
Publication date: 2024/02/29
Liu ZeyuJing ChuanqingZhang Wei - The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA). - Source: PubMed
Xu DongmeiLiu HuaDeng XiaoyuFu Jifan