Mad2L1 antibody
- Known as:
- Mad2L1 (anti-)
- Catalog number:
- orb100280
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- Mad2L1 antibody
Related genes to: Mad2L1 antibody
- Gene:
- MAD2L1 NIH gene
- Name:
- mitotic arrest deficient 2 like 1
- Previous symbol:
- -
- Synonyms:
- MAD2, HSMAD2
- Chromosome:
- 4q27
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-14
- Date modifiied:
- 2017-02-21
Related products to: Mad2L1 antibody
Related articles to: Mad2L1 antibody
- Population Attributable Fraction (PAF) is a key epidemiological measure used to quantify the contribution of risk factors to the overall disease burden. However, when an exposure affects an outcome through multiple ordered mediators, traditional PAF estimation methods face challenges in accurately identifying the impact of each mediating pathway. These challenges arise from mediator-outcome relationships, interactions among mediators, and the presence of potential confounders. In this study, we propose new measures, termed mPAFs, to quantify the fraction of disease attributable to a specific mediation pathway. The proposed framework incorporates a multiply robust estimator that yields consistent estimates of mPAFs provided that at least two of the three types of models are correctly specified: the exposure models, mediator models, or outcome model. The asymptotic properties of the estimator are formally established, and a comprehensive simulation study is conducted to demonstrate its robustness against model misspecification. In a real-data application using TCGA lung cancer cohorts, we analyzed the effect of smoking on mortality mediated through TTK and MAD2L1. In lung adenocarcinoma, the total PAF was estimated at 4.45%, with a direct effect of 1.82% and pathway-specific contributions of -1.95% (TTK) and 0.68% (MAD2L1). In contrast, lung squamous cell carcinoma showed a higher total PAF of 10.43%, with most of the effect attributable to the direct pathway (10.22%), suggesting minimal mediation via the selected genes. - Source: PubMed
Peng Han-ChiLee WoojooTai An-Shun - Liver hepatocellular carcinoma (LIHC) is a leading cause of cancer-related mortality worldwide, with limited therapeutic options and poor prognosis, particularly at advanced stages. Identifying key molecular drivers involved in LIHC progression is critical for improving diagnosis and treatment strategies. In this study, we performed an integrated bioinformatics analysis using four independent GEO datasets (GSE19665, GSE54236, GSE55092, and GSE84598) to identify differentially expressed genes (DEGs) associated with LIHC. A total of 147 common DEGs were identified, and protein-protein interaction network analysis revealed CCNA2, MAD2L1, AURKA, and PTTG1 as central hub genes. Functional enrichment analyses indicated that these genes are primarily involved in cell cycle regulation, mitosis, and chromosomal stability. Expression analyses using TCGA-based databases demonstrated significant upregulation of these hub genes at both mRNA and protein levels in LIHC tissues compared with normal liver tissues. Elevated expression was associated with advanced tumor stage, poor overall survival, immune cell infiltration, and altered drug sensitivity, highlighting their clinical relevance. Promoter methylation analysis suggested that epigenetic regulation may contribute to gene dysregulation, while genetic alterations were infrequent. Experimental validation using RT-qPCR confirmed overexpression of hub genes in LIHC cell lines. Furthermore, siRNA-mediated knockdown of these genes significantly suppressed proliferation, colony formation, and migration in HepG2 and Huh7 cells. Collectively, these findings identify CCNA2, MAD2L1, AURKA, and PTTG1 as key oncogenic drivers and potential biomarkers and therapeutic targets in LIHC. - Source: PubMed
Publication date: 2026/05/28
Jinli WangShiping Hu - Clutch length is a key determinant of reproductive efficiency in geese and strongly positively correlates with egg production. We recorded daily egg production in 280 individually housed Zi geese, calculated clutch-related indices, and selected 12 geese to form long-clutch (LC) and short-clutch (SC) groups for ovarian transcriptomic, proteomic, and metabolomic analyses. The results showed that egg number, large clutch length, large clutch number, average clutch length, and average clutch number were significantly higher in LC than in SC groups (P < 0.0001). Transcriptomic analysis identified 885 differentially expressed genes enriched in oocyte development and ovarian steroidogenesis, with APOB, PLA2G4C, MMP2, MMP9, and NOBOX as key genes; proteomic analysis identified 437 differentially abundant proteins enriched in arachidonic acid metabolism and mitophagy, with CXCL12, RARB, and MAD2L1 as key proteins; and metabolomic analysis identified 35 differentially abundant metabolites enriched in glycolysis/gluconeogenesis, with lactic acid, guanidinoacetic acid, and 3-hydroxybutyrylcarnitine as key metabolites. Integration of multi-omics datasets highlighted a lactate-associated cross-omics signature supported by YWHAZ at the protein level and by the lactate transporter SLC16A3. Collectively, these findings deepen our understanding of the molecular basis underlying clutch-length variation in goose ovaries and highlight candidate genes, proteins, and metabolites for future functional validation. - Source: PubMed
Publication date: 2026/03/02
Wang HechuanLiu YunuoJiang KeYin JiaxinCong KexinMiao XinyiYang WeiranZhang YingLiu Shengjun - HORMAD1 expression is usually restricted to germ-line cells but is also aberrantly expressed in 60% of triple-negative breast cancers (TNBCs), where it is bi-modally expressed and associated with genomic instability. Here, we show that out-of-context HORMAD1 expression in mitotic cells perturbs mitotic arrest and generates aneuploidy. These phenotypes are caused by out-of-context HORMAD1 expression driving a weakening of the spindle assembly checkpoint (SAC) and/or in kinetochore-microtubule error correction. These mitotic effects of HORMAD1 are MAD2L1-independent, but instead caused by a HORMAD1/Aurora B interaction and defective Aurora B/INCENP signalling. Consistent with this mechanism, aberrant HORMAD1 expression causes sensitivity to MPS1, Aurora B or BUB1 inhibitors currently being investigated as cancer treatments. Our data suggests how out-of-context expression of a meiotic gene imparts genomic instability upon tumour cells and also identifies several associated dependencies as mechanism-based therapeutic targets for a large, biomarker-defined, subset of cancers. - Source: PubMed
Publication date: 2026/03/11
Walker CallumKollarovic GabrielWeekes DanielTrendell JenniferHoffmann Ricarda MMartin AlexiaFerro RiccardoNavarro-Llinas BlancaHitchen LukePardo Calvo MercedesBalan NicolaeKemp HarrietCarroll AlexandraDavidson KathrynNath SarmiD'Uonno NadjaLu RuifangStarling ChrisOtten MariekeIakobachvili NinoMarcozzi ChiaraRahman IlhanQuist JelmarYu LuKrastev Dragomir BAmodeo ValeriaRoxanis IoannisGrigoriadis AnitaBayliss RichardChoudhary JyotiHaider SyedPines JonathonPettitt Stephen JLord Christopher JTutt Andrew N J - Hepatocellular carcinoma (HCC) remains one of the leading causes of cancer-related mortality worldwide, largely due to its insidious onset, aggressive progression, and limited therapeutic options, resulting in poor patient prognosis. The lack of reliable prognostic biomarkers has significantly impeded precise patient stratification and personalized treatment. - Source: PubMed
Publication date: 2025/11/18
Song HongWang XiangyuQin YunpengYang WantingCheng ZhenYang JianhuaYang PeizhengYan BiaobiaoWu ZiyinSheng HaiyangYang YinfengYang XiangyuWang Jinghui