CCND1 ELISA kit
- Known as:
- CCND1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CCND1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CCND1 ELISA kit
Related genes to: CCND1 ELISA kit
- Gene:
- CCND1 NIH gene
- Name:
- cyclin D1
- Previous symbol:
- BCL1, D11S287E, PRAD1
- Synonyms:
- U21B31
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2019-04-23
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- Myocardial fibrosis represents a critical prognostic indicator of poor outcomes in hypertrophic cardiomyopathy (HCM), frequently predisposing patients to lethal ventricular arrhythmias and progressive heart failure. However, the upstream molecular mechanisms driving cardiac fibrogenesis in HCM remain largely unresolved. This study aimed to identify key fibrotic pathways and regulatory genes in HCM patients using weighted gene co-expression network analysis (WGCNA). - Source: PubMed
Publication date: 2026/09/25
Chang LeiGong ChenyiWu ZhikangWang LianShen Qiannan - Psoriasis is a chronic skin disease manifesting scaly, indurated erythema and an enhanced interleukin (IL)-23/IL-17 immune axis. A high-salt diet (HSD) is known to promote several autoimmune or autoinflammatory diseases. We examined whether an HSD might exacerbate topical imiquimod (IMQ)-induced psoriasis-like dermatitis in mice. Balb/c female mice were fed a normal diet (ND, 0.2% NaCl) or an HSD (4.2% NaCl) for 3 weeks, and 25 mg IMQ was applied to shaved back skin for 5 consecutive days. Compared to ND, the HSD exacerbated IMQ-induced psoriasiform dermatitis with increased scale, skin thickness, and total scores, and histologically enhanced epidermal thickening, hyperkeratosis, and dermal inflammatory infiltrates, including Ly6G+ neutrophils and CD3+ T cells. HSD increased mRNA levels of , , , , , , , , , and in IMQ-induced dermatitis. HSD increased the immunostaining areas of whole and Ser 422-phosphorylated forms of serum- and glucocorticoid-inducible kinase 1 (SGK1) in epidermal keratinocytes and dermal-infiltrating cells in IMQ-induced dermatitis. Intraperitoneal SGK1 inhibitor EMD638683 reversed the above effects of HSD in exacerbating IMQ-induced dermatitis. Our present results indicate that HSD may exacerbate murine IMQ-induced psoriasis-like dermatitis at least partially through the activation of SGK1. - Source: PubMed
Publication date: 2026/09/13
Yoshida MaiHagino TeppeiYoneyama ManamiSaeki HidehisaKanda Naoko - Mexico has one of the highest incidences of childhood acute lymphoblastic leukemia worldwide and also reports one of the lowest 5-year overall survival rates; one cause is elevated treatment-related mortality from severe hematologic toxicity, a critical side effect during chemotherapy. Although association studies have identified common genetic variants linked to toxicity, the Mexican population remains incompletely explored. We performed targeted next-generation sequencing of genes involved in methotrexate and mercaptopurine metabolism in 96 Mexican children with ALL, stratified by hematologic toxicity severity according to CTCAE v5.0. Logistic regression revealed nominally significant associations between the genotype (rs45445694) in the 5' UTR of severe hematologic toxicity (overdominant model: OR = 3.21; 95% CI = 1.23-8.38; = 0.014 and codominant model: OR = 3.31; 95% CI = 1.17-9.34; = 0.047). Additionally, the LD block (rs678653/rs7177) also showed nominal associations (overdominant model: OR = 2.60; 95% CI = 1.01-6.71; = 0.044). None of these associations remained statistically significant after Bonferroni correction for multiple testing (corrected α = 0.000588). Patients with severe toxicity had lower 5-year overall survival than those without severe toxicity (70.2% vs. 90.5%; = 0.0609), although the difference was not statistically significant. Variants in 5' and 3' UTRs regions were markedly enriched compared to coding sequences, underscoring the importance of regulatory region analysis. - Source: PubMed
Publication date: 2026/09/12
Rojo-Serrato DanielaFlores-Murrieta Francisco JavierRosas-Vargas HaydeéJiménez-Hernández ElvaNúñez-Enríquez Juan CarlosGonzález-Torres CarolinaGaytan-Cervantes JavierEscalante-Bautista DeyaniraPérez-Saldivar María LuisaFlores-Lujano JanetJasso-Mata América MarianaMarquez-Águilar Abimael EfraínSotelo Hernández José ÁngelSepúlveda-Robles Omar AlejandroRomero-Tlalolini María de Los ÁngelesAlaez-Verson CarmenMartín-Trejo Jorge AlfonsoJiménez-Morales SilviaCruz-Jaramillo José LuisAnda Norma A Oviedo deCastillo-Mendéz Manuel ATorres-Nava José RefugioFlores-Villegas Luz VictoriaMerino-Pasaye Laura ElizabethMiranda-Madrazo María RaquelGutiérrez-Rivera María de LourdesSolís-Labastida Karina AnatasiaHerández-Echaurregui Gabriela AliciaMelendez-Zajgla JorgeRangel-López AngélicaArellano-Galindo JoséMata-Rocha MinervaMejía-Aranguré Juan Manuel - Cancer remains a major global health concern, driving the search for safe and effective bioactive compounds from natural sources. Jujube peel red pigment (JP), an anthocyanin-rich extract, has shown preliminary bioactivity, yet its antitumor potential and delivery challenges remain underexplored. This study systematically evaluated the in vitro antitumor activity of JP and developed a thermosensitive hydrogel-based local delivery system (JP-H) to overcome its rapid diffusion and poor retention. JP exhibited selective cytotoxicity against HeLa cervical cancer and B16 melanoma cells, with no obvious toxicity to normal L929 and RAW264.7 cells. In HeLa cells, JP exerted antitumor effects by initiating mitochondrial-dependent apoptosis accompanied by elevated expression of Bax and cleaved Caspase-9/-3 as well as decreased Bcl-2 level, and arrested cell cycle at the G1/S phase by regulating CCND1, CDK2, CDK4, PCNA, MYC and TP53. To enable localized delivery, JP was incorporated into an injectable chitosan/gelatin/F127 thermosensitive hydrogel (JP-H), which exhibited rapid sol-gel transition at physiological temperature, shear-thinning behavior, and a porous microstructure. JP-H not only sustained JP release but also significantly enhanced antibacterial activity against and compared to free JP. Furthermore, JP-H markedly inhibited HeLa cell migration and induced superior apoptotic/necrotic cell death in co-culture assays, outperforming free JP. Collectively, this work establishes JP as a multi-target antitumor agent and demonstrates JP-H as a promising local therapeutic platform combining sustained delivery, antibacterial protection, and enhanced anticancer efficacy for cervical cancer treatment. - Source: PubMed
Publication date: 2026/09/01
Zhang PeiChen QianqianChen ShichaoGuo HuixiaMa MengruPu YugeJiang ZhenchaoLiu HongxiaGuo PeiranZhao XushengZhang YingYang Xueyi - Premature ovarian insufficiency (POI) affects female fertility; however, the mechanisms are not yet fully understood. The aim of this study was to investigate the relationships among bisphenol A (BPA), microRNAs (miRNAs), and the cell cycle-related protein Cyclin D1 (CCND1) in ovarian granulosa cells. Using cell culture and transfection techniques, we analysed the effects of BPA on the proliferation of ovarian granulosa cells. Concurrently, qRT‒PCR and Western blotting were employed to assess miRNA expression levels and CCND1 protein levels, respectively. Our results demonstrated that BPA significantly inhibited the proliferation of ovarian granulosa cells. This inhibition was closely associated with the upregulation of specific miRNA expression and the downregulation of CCND1 protein expression. Furthermore, the overexpression of the identified miRNAs partially reversed the BPA-induced changes in CCND1 expression. These findings reveal a potential role for BPA in POI pathogenesis through the regulation of miRNAs and the cell cycle protein CCND1, providing a novel perspective on the mechanisms underlying this disorder. Future research should further elucidate the specific roles of these miRNAs and CCND1 in ovarian insufficiency and explore their potential application as therapeutic targets. - Source: PubMed
Publication date: 2026/09/25
Du ErqiuPan JinZhang LingXu Wei