DOM3Z Blocking Peptide
- Known as:
- DOM3Z Blocking Peptide
- Catalog number:
- 33r-5573
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- DOM3Z Blocking Peptide
Related genes to: DOM3Z Blocking Peptide
- Gene:
- DXO NIH gene
- Name:
- decapping exoribonuclease
- Previous symbol:
- DOM3Z
- Synonyms:
- -
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-16
- Date modifiied:
- 2016-10-05
Related products to: DOM3Z Blocking Peptide
Related articles to: DOM3Z Blocking Peptide
- Chemotherapy can compromise the fertility of boys with cancer, yet no standard protocols exist to preserve their reproductive potential. Before puberty, germ cells are almost exclusively spermatogonia that can be the target of anticancer drugs. Doxorubicin (DXO), a widely used anthracycline in pediatric oncology, has been associated with infertility in adulthood, but its immediate effects on prepubertal germ cells remain poorly understood. In the present study, a preclinical rat model of prepubertal DXO exposure was developed to characterize the mechanisms underlying immediate DXO-induced germ cell damage. Six-day-old pups, received a single intraperitoneal injection of DXO (5 mg/kg) and effects were measured after 24 or 48 h. DXO exposure significantly reduced relative testis weight from 24 h and significantly increased apoptosis and germ cell loss at 48 h, while circulating testosterone remained unchanged, suggesting a selective germline effect. RNA-seq was done on GFP-positive germ cells purified at 24 h. Transcriptomic analysis confirmed the enrichment in spermatogonial stem cells (SSCs) in the GFP-sorted population. Moreover, DXO induced 51 differentially expressed genes (49 upregulated, 2 down regulated) that were mostly related the p53-dependant apoptosis pathway. Pro-apoptotic genes (Cdkn1a, Bbc3/Puma, Tp53inp1, Fas) and oxidative stress regulators (Sesn2, Eda2r, Abhd4) were induced, whereas DNA repair genes (Mgmt, Xrcc1, Polh, Gadd45α, …) were not activated. Our data revealed the DXO-induced immediate transcriptomic response after 24 h, leading to germ cell death observed by histology at 48 h. These findings suggest that SSCs respond to DXO by favoring apoptosis and stress regulation, a strategy that may preserve germline integrity and reduce the risk of transmitting genetic damage to the next generation. - Source: PubMed
Publication date: 2026/02/28
Beaud HermanceHug ElisaScott-Boyer Marie-PierRwigemera ArletteTremblay AmélieDroit ArnaudDelbes Géraldine - Obesity exhibits a high heritability with heterogeneity; however, the genetic variants identified as obesity-causing factors are still underexplored. By performing deep sequencing on 2295 cases of young-onset obesity from East Asian populations and 2292 lean controls, we identified five genes (, , , , and ) with an excess burden of rare predicted loss-of-function (LoF) variants in cases. Among the variants, TUB p.R364G was identified as a potential deleterious variant that disrupted TUB protein's subcellular localization. Knock-in mice carrying the homologous p.R363G variant exhibited hyperphagia and obesity in an allele dose-dependent manner when fed a high-fat diet. The TUB p.R363G variant also blunted responses to leptin-induced suppression of food intake, leading to leptin resistance in mice. Furthermore, we demonstrated that TUB acted as a positive regulator of the leptin pathway through its interaction with STAT3, and this interaction was impaired by the p.R364G variant. TUB silencing mitigated the inhibitory effects of leptin on the activities of agouti-related protein (AgRP)-expressing neurons. Consistently, conditional ablation of TUB in AgRP neurons in mice led to hyperphagic obesity and attenuated leptin-induced appetite suppression in mice. Thus, our study demonstrates that rare LoF variants in TUB predispose to young-onset obesity in humans, likely through impairing leptin sensitivity in AgRP neurons. - Source: PubMed
Publication date: 2026/02/11
Tong MuyeChen YanruSong BeiteHong JieGu WeiqiongShen JuanYang HuanjieXia HuiminLi QianChen YufeiZhao ShaoqianLyu QianqianXue WenzhiMa QinyunZhou HoudeWu HuixuanGuo YihuaCao ZhiwenZhao YuxiaoZhang MinchunGu XuejiangZheng JieZhang YifeiLu JieliNing GuangBi YufangWang WeiqingLiu RuixinWang Jiqiu - Dialysis nurses routinely make high-stakes clinical decisions under conditions of uncertainty, balancing protocol-based guidelines with contextual and experiential judgment. Recent advances in artificial intelligence (AI) raise questions regarding its potential role in supporting nursing clinical reasoning. - Source: PubMed
Publication date: 2026/01/31
Orkaby BruryaSegev RonenSaban Mor - The high incidence of respiratory diseases has driven a substantial increase in the use of antitussive dextromethorphan (DXM), leading to the frequent detection of its primary human metabolite, dextrorphan (DXO), in aquatic environments. However, existing research has paid limited attention to the toxic effects of DXM and its metabolite, DXO, on fish. In this study, zebrafish embryos were exposed to DXM and DXO at concentrations ranging from 100 to 10,000 ng/L for 72 hours post-fertilization (hpf) to evaluate their impacts on cardiac function and elucidate underlying molecular mechanisms using network toxicology and molecular dynamics approaches. Bradycardia was observed at 48 hpf. By 72 hpf, key cardiac morphometric and functional indices, as well as blood flow, exhibited concentration-dependent suppression after exposure to DXM and DXO. Network toxicology analysis revealed that the beta2-adrenergic receptor () was the key common target in cardiomyocyte adrenergic signaling for both compounds. Further observations included significant downregulation of , decreased levels of beta2-adrenergic receptor and protein kinase A proteins, and phenotypic rescue after coexposure to adrenaline. The binding energies of DXM and DXO to the beta2-adrenergic receptor were -23.45 and -25.76 kcal/mol, respectively. These findings confirmed that DXM and DXO impaired cardiomyocyte function via suppression of beta2-adrenergic receptor expression, leading to bradycardia. It is worth noting that DXO exhibited stronger cardiac toxicity than its parent compound DXM, and its ecological toxicity warrants special attention and further evaluation. - Source: PubMed
Publication date: 2026/01/30
Cao ZhouLiang ZhuZhang Jin-GeMa Dong-DongMeng Yun-ZeLu Zhi-JieShi Wen-JunYing Guang-Guo - Dextromethorphan/Buproprion (DXM/BUP) has received breakthrough FDA approval in August 2022 as a rapid-acting antidepressant. DXM/BUP is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist and sigma-1 receptor agonist, with bupropion (BUP), a norepinephrine/dopamine reuptake inhibitor and cytochrome P450 2D6 (CYP2D6) inhibitor. As DXM/BUP moves closer to widespread clinical use for MDD, examining whether the combination does or does not carry meaningful abuse liability is essential given that DXM alone has long been misused, likely attributed to its metabolism into the psychoactive metabolite DXO. - Source: PubMed
Publication date: 2025/12/24
Zheng Yang JingDri Christine EWong SabrinaLe Gia HanTeopiz Kayla MKwan Angela T HMcIntyre Roger S