Ask about this productRelated genes to: MAD1L1 antibody
- Gene:
- MAD1L1 NIH gene
- Name:
- mitotic arrest deficient 1 like 1
- Previous symbol:
- -
- Synonyms:
- HsMAD1, TXBP181, MAD1, PIG9, TP53I9
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-07
- Date modifiied:
- 2017-09-12
Related products to: MAD1L1 antibody
Related articles to: MAD1L1 antibody
- Triple-negative breast cancer (TNBC) is frequently characterized by notably elevated Ki-67 expression, a hallmark of uncontrolled rapid cell-cycle progression. However, the underlying mechanisms remain unclear, leading to limited therapeutic options. - Source: PubMed
Publication date: 2026/04/22
Liu NianqiuZhu MengdiCai ZijieWang JingruCao WeihanShi QianfengWang LinghanJiang XiaotingZhou JingLin JinnaYang WangGan HuipeiNie JianyunLiu Qiang - Cisplatin (DDP) resistance remains a major therapeutic obstacle in non-small-cell lung cancer (NSCLC). Tumor-associated macrophages (TAMs) are known to promote chemoresistance via exosomal signals, but whether exosomal long non-coding RNA NEAT1 contributes to this process is unclear. In this study, we found that exosomes derived from DDP-treated macrophages were enriched with NEAT1 and delivered it to A549 cells. This transfer enhanced the DNA damage response, promoted cell-cycle progression, and reduced DDP-induced apoptosis. Through RNA-sequencing and luciferase reporter assays, we identified MAD1L1 as a key downstream target of NEAT1. NEAT1 was enriched at the MAD1L1 promoter, upregulated its expression, and subsequently suppressed the p53/p21/Bax axis, thereby fostering a chemoresistant phenotype. , exosomal NEAT1 promoted tumor growth in DDP-treated xenografts, while NEAT1 knockdown reversed this effect and restored p53 pathway activity. Collectively, our work unveils a novel TAM-exosome-NEAT1-MAD1L1/p53 signaling axis that drives cisplatin resistance in lung adenocarcinoma, highlighting NEAT1 and its intercellular delivery as potential therapeutic targets to overcome chemoresistance. - Source: PubMed
Publication date: 2026/03/25
Yang YiMeng MinZhao YiYu FangyuanPatel HarshChen Zhe-Sheng - Evidence linking secondhand tobacco exposures to childhood attention-deficit hyperactivity disorder (ADHD) risk has been reported, however, the causality of the relationship and potential biological pathways is unknown. We applied a two-step Mendelian randomisation (MR) analysis and Bayesian colocalization analysis to examine the causal relationship between smoking behaviours, secondhand tobacco-induced DNA methylation and childhood ADHD risk. The findings revealed causal positive connections between smoking behaviours of daily cigarette consumption (Odds ratio [OR]Inverse variance weighted (IVW), 1.56 for per 1–SD increase; 95% CI: 1.17–2.09; P = 0.003), smoking cessation (ORIVW, 2.92 for per 1–SD increase; 95% CI: 1.65–5.17; P = 2.23 × 10− 4), smoking initiation (ORIVW, 3.01 for per 1–SD increase; 95% CI: 2.60–3.48; P = 6.41 × 10− 50) and the risk of childhood ADHD. On the contrary, age of initiation of regular smoking suggested a decreased risk with ADHD risk (ORIVW, 0.17 for per 1–SD increase; 95% CI: 0.06–0.47; P = 7.42 × 10− 4). Genetically predicted DNA methylation alterations related to secondhand tobacco exposure at cg23211703 [PTPRF], cg02772619, cg19716073 [CACNG1], and cg22500280 [MAD1L1] were associated with increased ADHD risk, whereas DNA methylation changes at cg03504834 [FOXP2], cg23666170 [PLK1S1], cg24476096 [C1orf84/MED8], cg12142869 [OR10AD1] and cg16572910 were related to decreased ADHD risk. Five CpG sites (cg23211703, cg03504834, cg02772619, cg12142869, and cg19716073) exhibited convincing colocalization evidence. This study provides evidence supporting a causal link between tobacco smoking, DNA methylation and childhood ADHD risk. - Source: PubMed
Publication date: 2026/04/07
Shang KeleiLuo ChunTan XiaoguangXu MengleiLi BinWang HouhongCheng Feng - Germ cell tumors (GCTs) are heterogeneous neoplasms arising from primordial germ cells. While genome-wide association studies (GWAS) have identified numerous susceptibility loci for adult testicular GCTs (TGCTs), the heritable basis of pediatric TGCT and GCTs that arise outside the testes remain poorly understood. - Source: PubMed
Publication date: 2026/03/30
Sullivan Shannon MLane JohnStandafer AbigailMcfeeters JamesHubbard Aubrey KLanger Erica KHooten Anthony JRoesler Michelle AGell Joanna JKrailo MarkFrazier A LindsayAmatruda James FPankratz NathanPoynter Jenny N - Mad1 is an essential component of the mitotic spindle assembly checkpoint. During interphase, Mad1 regulates the trafficking of α5 integrin from the Golgi to the plasma membrane. Here, we show that depletion of Mad1 or α5 integrin induces cytokinesis failure. Though the cytokinetic furrow ingresses with normal timing, it ultimately regresses, resulting in cytokinesis failure. We identify an ~300 amino acid internal fragment of Mad1 that is necessary and sufficient for the Golgi localization of Mad1. This fragment, which we term Mad1-Golgi, can rescue α5 integrin secretion and cytokinesis in Mad1-depleted cells. Expression of exogenous α5 integrin is sufficient to overcome the cytokinesis defect caused by Mad1 depletion. The contribution of both Mad1 and α5 integrin to cytokinesis is observed specifically under adherent growth conditions, and a pool of both proteins localizes to the midbody in adherent cells. These results demonstrate a previously uncharacterized role for Mad1 in cytokinesis by regulating α5 integrin secretion from the Golgi apparatus. - Source: PubMed
Publication date: 2026/03/30
Sam Daniel KGrems GretaAudhya AnjonWeaver Beth A