MCM4 antibody - middle region (ARP36649_T100)
- Known as:
- MCM4 (anti-) - middle region (ARP36649_T100)
- Catalog number:
- arp36649_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MCM4 antibody - middle region (ARP36649_T100)
Related genes to: MCM4 antibody - middle region (ARP36649_T100)
- Gene:
- MCM4 NIH gene
- Name:
- minichromosome maintenance complex component 4
- Previous symbol:
- CDC21
- Synonyms:
- CDC54, hCdc21, P1-Cdc21, MGC33310
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
Related products to: MCM4 antibody - middle region (ARP36649_T100)
Related articles to: MCM4 antibody - middle region (ARP36649_T100)
- Hereditary adrenocortical unresponsiveness to adrenocorticotropin (HAUA) is a rare congenital disorder characterized by isolated glucocorticoid deficiency with preserved mineralocorticoid production. HAUA encompasses familial glucocorticoid deficiency (FGD) and triple A syndrome (AAAS) and is caused by autosomal recessive defects in ACTH-signaling-related genes, including MC2R, MRAP, AAAS, NNT, TXNRD2, and MCM4. To clarify the current clinical characteristics of HAUA (including FGD and AAAS) in Japan, we conducted a nationwide questionnaire-based survey. The primary survey identified the number of affected patients, and the secondary survey collected detailed clinical information. Fifteen patients were identified from 12 institutions. Detailed clinical data were obtained from nine patients (mean age, 40.6 years). Most patients developed symptoms during childhood [3.75 (0-8) years]. Seven presented with chronic adrenal insufficiency, and two experienced life-threatening events, hypoglycemia or encephalopathy. Genetic confirmation was obtained in four cases. All patients received glucocorticoid replacement therapy (mean hydrocortisone-equivalent dose, 13.0 mg/m/day). Notably, 50% of adult patients were obese (BMI ≥25 kg/m), although no clear association between glucocorticoid dose and BMI was observed. Despite the limited cohort size, this study provides detailed clinical information on HAUA (including FGD and AAAS) in Japan and suggests a potential risk of obesity in long-term management. - Source: PubMed
Publication date: 2026/08/11
Tanimoto EriKashimada KenichiMatsuura BunzoYamaguchi HidekiKurajoh MasafumiSegawa ToshieOhba KenjiAbe YukiWada YasunoriKanno JunkoOda YoichiroTajima ToshihiroShibata HirotakaHasegawa Tomonobu - Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive disorder characterized by isolated cortisol deficiency and elevated adrenocorticotropic hormone (ACTH) levels. Variants in , which encodes mitochondrial thioredoxin reductase 2, have recently been implicated in FGD; however, the phenotypic and mutational spectrum remain extremely limited. - Source: PubMed
Publication date: 2026/05/28
Al Alwan IbrahimAlhamoudi Kheloud MAlzaben Abdullah IbrahimAlmulhem BeshaierQawasmi NawalAlswailem MeshaelAlotaibi SaraAlsaihati BurairJabaan AmjadMahzari MoeberFlück Christa EAlzahrani Ali S - Gastric cancer (GC) is the fifth leading cause of cancer-related mortality worldwide. Treatment options for advanced GC remain limited, owing to the frequent emergence of drug resistance. This highlights an urgent clinical need for novel therapeutic targets. Abnormal energy metabolism is a hallmark feature of cancer. MYC_V1-driven metabolic reprogramming plays a pivotal role in tumor progression. However, the specific mechanisms by which MYC_V1-related genes regulate energy metabolism in GC remains poorly understood. We employed single-sample gene set enrichment analysis (ssGSEA) to evaluate multiple tumor hallmarks in GC. A prognostic risk model was constructed based on MYC_V1-related genes, with the risk score (RS) used to stratify patients into distinct risk groups. A nomogram was developed and validated using calibration curves. Through the systematic molecular docking screening of 8327 compounds, potential therapeutic agents were identified. Functional experiments, including the CCK-8 assay, wound-healing assay and ATP production assay, were conducted to validate the role of in GC progression. This study identified MYC_V1 as the primary risk factor affecting the overall survival (OS) in GC patients ( = 0.038). A prognostic risk model was successfully constructed based on eight MYC_V1-related genes (, , , , , , , and ). The RS was confirmed as an independent prognostic factor. The prognostic risk model accurately predicted patient 1-, 3-, and 5-year OS in GC patients. Tumor microenvironment analysis revealed significant differences in immune cell infiltration patterns between high-risk and low-risk groups. High-throughput drug screening and molecular docking identified camptothecin (CPT) and vinblastine as showing strong therapeutic potential for high-risk patients. Experimental validation demonstrated that was significantly overexpressed in GC tissues, and its knockdown markedly suppressed the proliferation, migration capacity, and intracellular ATP production in GC cells, confirming the critical role of in GC progression. These findings establish as a potential therapeutic target in GC. - Source: PubMed
Publication date: 2026/05/28
Xu DuoPeng LingyiHe JingWang XueXia Jiaqi - Castration-resistant prostate cancer (CRPC) is a fatal malignancy often associated with alterations in cell cycle regulation, particularly within the Cyclin/CDK/RB axis. Despite ongoing clinical trials assessing CDK4/6 inhibitors in prostate cancer, clinical evidence remains limited. Although the androgen receptor (AR) inhibitor enzalutamide (ENZ) initially demonstrates therapeutic efficacy, resistance develops over time, and monotherapy offers limited antitumor benefits, highlighting the need for effective combination therapies. In this study, pharmacological profiling, genetic dependency analysis, RNA sequencing, and functional validation were conducted across various in vitro and in vivo preclinical CRPC models. The combination of ENZ and the CDK4/6 inhibitor dalpiciclib (DAL) exhibited potent antitumor activity in CRPC cell lines, a cell-derived xenograft (CDX) model, and a lymphatic metastatic model. Moreover, ENZ plus DAL inhibited cell cycle progression, migration, and DNA replication, while promoting apoptosis in CRPC cells. Mechanistically, ENZ blocked AR-mediated transcriptional activation of MCM4, a critical component of the DNA helicase complex, thereby enhancing the effect of CDK4/6 inhibition on DNA replication and inducing a pronounced synergistic antitumor response. These results suggest that the ENZ-DAL combination is a promising therapeutic approach that warrants further clinical evaluation in CRPC patients. - Source: PubMed
Publication date: 2026/06/05
Liu YueKe YuanYu JingtianChai MengtingZheng LinhuiYang ChunqianLiu DongCheng ShiyuXiong ZhiyuanFeng JialiangZhao ZhenpengWu ChaoyanYu Haijun - Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer worldwide, with increasing incidence and mortality rates. Although several targeted therapies are currently available, the therapeutic outcomes remain unsatisfactory due to the high heterogeneity and drug resistance of HCC. Therefore, novel molecular mechanisms and therapeutic strategies urgently need to be explored. In this study, we obtained the GSE39791 dataset from the GEO database and identified 1,186 differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) was conducted to obtain 776 key module genes, which were intersected with 11,671 HCC-related genes from the GeneCards database, resulting in 226 candidate genes. A protein-protein interaction (PPI) network was constructed using the STRING database, and the top 20 hub genes were identified using the MNC algorithm in Cytoscape. Among these, the five most significant hub genes-RFC4, TOP2A, AURKA, HSP90AA1, and MCM4-were selected for further analysis. KEGG enrichment analysis was performed to explore their functional pathways. Potential therapeutic agents were predicted using the CMap database, and molecular docking was conducted via AutoDock Vina. To validate the computational predictions, a quercetin intervention model was established. The optimal dose was determined through CCK-8 assays in HepG2 cells, and the expression of the five hub genes was examined in normal liver cells (LO2), HepG2 cells, and HepG2 cells treated with quercetin using RT-qPCR. The five hub genes-RFC4, TOP2A, AURKA, HSP90AA1, and MCM4-were significantly overexpressed in both HCC tissues and cell lines. Enrichment analysis revealed that these genes were mainly involved in cancer-related pathways, including the cell cycle, p53 signaling pathway, and FoxO signaling pathway. Drug prediction analysis showed that quercetin exhibited a negative regulatory pattern with respect to HCC and displayed binding energies below - 5 kcal/mol with all five hub proteins. CCK-8 assays confirmed the dose-dependent inhibitory effect of quercetin on HepG2 cell viability. RT-qPCR results demonstrated that quercetin significantly downregulated the expression of the five hub genes, consistent with the bioinformatics predictions. This study integrated multi-omics analysis and experimental validation to identify five core genes closely associated with HCC and suggested that quercetin may exert anti-HCC effects partly associated with the regulation of these genes. Our findings offer new insights into the molecular mechanisms of HCC and provide a promising strategy for the development of targeted therapeutics. - Source: PubMed
Publication date: 2026/05/14
Zeng LongfeiZhu GangTang ShaozhenWu TaoYang LiuZhang XinDai Li