Ask about this productRelated genes to: ATP6V0D2 Blocking Peptide
- Gene:
- ATP6V0D2 NIH gene
- Name:
- ATPase H+ transporting V0 subunit d2
- Previous symbol:
- ATP6D2
- Synonyms:
- FLJ38708, VMA6
- Chromosome:
- 8q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-09
- Date modifiied:
- 2017-03-10
Related products to: ATP6V0D2 Blocking Peptide
Related articles to: ATP6V0D2 Blocking Peptide
- BackgroundEarly diagnosis of chronic obstructive pulmonary disease (COPD) remains challenging due to the limited sensitivity of spirometry and imaging in early-stage disease and the lack of reliable blood-based biomarkers. COPD is increasingly recognized as a heterogeneous disorder driven by coordinated immune dysregulation and airway structural remodeling; however, clinically applicable molecular signatures that capture these processes are still lacking.ObjectivesTo identify and validate a blood-based diagnostic signature for COPD and to explore the underlying immune and structural remodeling mechanisms.DesignA multi-stage integrative study combining retrospective bioinformatics analysis with prospective experimental validation.MethodsPublic lung transcriptomic datasets were used to identify COPD-associated candidate genes through differential expression, co-expression network, and machine-learning analyses. Candidate genes were validated by RT-qPCR in peripheral blood samples from stable COPD patients and healthy controls. Exploratory immune, single-cell, virtual perturbation, and molecular simulation analyses were performed to assess potential biological relevance.ResultsFour lung-derived candidate genes, AC079767.4, CEP55, EMR3, and ATP6V0D2, were identified. In peripheral blood validation, CEP55 and ATP6V0D2 showed the strongest diagnostic performance, whereas AC079767.4 showed limited blood-based discriminatory ability. Functional and immune analyses suggested that these genes may be associated with intracellular pH regulation, vesicular acidification, cytokinesis, immune imbalance, and inflammatory pathways. Single-cell analysis indicated that CEP55 was mainly enriched in epithelial, endothelial, and smooth muscle cells, whereas ATP6V0D2 was enriched in macrophages and monocytes. Virtual perturbation and molecular simulation analyses provided hypothesis-generating evidence for possible involvement in antigen presentation, T-helper-cell-related pathways, and ligand-target interactions.ConclusionThis study identified four lung-derived COPD-associated candidate genes through integrative transcriptomic, network, and machine-learning analyses. Among them, CEP55 and ATP6V0D2 showed the strongest peripheral-blood diagnostic performance and biological plausibility, supporting their prioritization as candidate circulating biomarkers for further validation. Exploratory docking and MD simulations suggested possible ligand-target interactions involving CEP55 and ATP6V0D2, but these computational findings require experimental pharmacological validation before any therapeutic relevance can be inferred. - Source: PubMed
Publication date: 2026/08/22
Du WenboWang YukunLi XiangWang RuiruiTong Shuping - To explore the mechanism of Pill (LWDHW) for improving postmenopausal osteoporosis (PMOP). - Source: PubMed
Zheng RuoxiXie LihuaHuang XiaobinGe Jirong - Although hydrophobic drugs demonstrate the promising therapeutic efficacy for peripheral artery disease , their performance is often hindered by low bioavailability due to inherent hydrophobicity. To address this, an injectable, self-healing and curcumin-sustained-release hydrogel (CGP hydrogel) using a gelatin/polyvinyl alcohol hydrogel (GP hydrogel) was developed. The CGP hydrogel effectively preserved the DPPH radical-scavenging activity of curcumin at room temperature. Meanwhile, in the murine hindlimb ischemia model, a single intramuscular injection of CGP following femoral artery ligation significantly improved the motor function of the ischemic limb compared to curcumin suspension. This superior therapeutic outcome is attributed to the sustained release of curcumin from the CGP hydrogel. Mechanistically, we found that CGP, but not GP, inhibited the expression of in ischemic skeletal muscle cells and suppressed ischemia-induced autophagy. The inhibition of autophagy may mitigate tissue and cellular necrosis and promote the expression of Myogenin. Furthermore, CGP reduced the expression of pro-fibrotic factors such as and and prevented skeletal muscle fibrosis. In summary, the CGP hydrogel, through its sustained release of curcumin, inhibits ischemia-induced autophagy, alleviates necrosis and fibrosis in skeletal muscle tissue and preserves motor function in the ischemic limb. - Source: PubMed
Publication date: 2026/07/02
Tang HanfeiWang FangHan TongleiLiu XuanyongLi MinhuiZhu JiaqiTang XiaoLiu GuoweiQiu JiajunGuo Daqiao - Estrogen deficiency-induced osteoporosis is largely driven by excessive osteoclast formation and bone resorption, but the direct pharmacological targets of flavonoid derivatives in osteoclast differentiation remain unclear. Here, we investigated the anti-osteoclastogenic activity and molecular mechanism of 2'-O-Galloylhyperin (2'-O-GH), a structurally defined flavonoid derivative. The effects of 2'-O-GH on RANKL-induced osteoclastogenesis were evaluated in bone marrow-derived macrophages and RAW264.7 cells using TRAP staining, qPCR, western blotting, F-actin staining, immunofluorescence, and bone resorption assays. Target identification was performed using a biotinylated 2'-O-GH probe coupled with pull-down and LC-MS/MS analysis, followed by molecular docking and microscale thermophoresis. In vivo efficacy was assessed in an ovariectomy-induced osteoporosis mouse model. 2'-O-GH inhibited RANKL-induced formation of TRAP-positive multinucleated osteoclasts without evident cytotoxicity at effective concentrations. It downregulated osteoclast-related markers, including NFATc1, c-FOS, SRC, ACP5, ATP6V0D2, and CTSK, and impaired F-actin ring formation and bone resorption. Mechanistically, 2'-O-GH restrained RANKL-induced NF-κB p65 nuclear translocation. Chemical proteomics identified MAP3K11/MLK3 as a candidate target, and molecular docking and microscale thermophoresis supported its direct interaction with 2'-O-GH. 2'-O-GH further suppressed RANKL-induced phosphorylation of MLK3 and IKKα/β, whereas MLK3 overexpression partially rescued NF-κB activation and osteoclast differentiation. In ovariectomized mice, 2'-O-GH attenuated bone loss without obvious effects on body or uterine weight. These findings identify MLK3 as a pharmacological target of 2'-O-GH and suggest that 2'-O-GH suppresses osteoclastogenesis through the MLK3/IKK/NF-κB axis. - Source: PubMed
Publication date: 2026/08/06
He GaoluChen RuihanFang ZhiyuFu SiyiWang YuzheLi HengzhiHu PengfeiBao JiapengRan Jisheng - leaf extract (ELE) boasts a high concentration of bioactive components including flavonoids, chlorogenic acid, and polysaccharides. It exhibits multiple biological functions, including antioxidant, anti-inflammatory, and gut microbiota-modulating properties, showing great potential in enhancing immunity, maintaining intestinal health, and delaying cellular senescence. This study investigated the protective effects and underlying mechanisms of ELE against D-galactose-induced senescence in chick embryo primary intestinal epithelial cells (IECs). Using an in vitro model (200 mmol/L D-galactose), we found that 100 µg/mL ELE pretreatment significantly preserved cell viability, mitigated apoptosis, and delayed cellular senescence, as evidenced by cytological and biochemical assays. Furthermore, RNA-seq transcriptomic analysis identified seven key differentially expressed genes (DEGs) mediating these anti-aging effects. Mechanistic investigations revealed that ELE modulates ATP6V0D2 and NCF2 to activate autophagy signaling pathways. This ELE-induced promotion of autophagy effectively suppresses inflammatory responses in IECs, thereby delaying senescence progression. These findings elucidate the molecular mechanisms by which ELE antagonizes intestinal cellular senescence, providing a solid theoretical foundation for its development as a functional anti-aging additive in the food industry. - Source: PubMed
Publication date: 2026/07/16
Liang XiaoxiaoCheng YiruWang RuxiaWang QianTang PengYin YulongXiong Xia