ADRa2C ELISA kit
- Known as:
- ADRa2C Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADRa2C-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADRa2C ELISA kit
Related genes to: ADRa2C ELISA kit
- Gene:
- ADRA2C NIH gene
- Name:
- adrenoceptor alpha 2C
- Previous symbol:
- ADRA2L2, ADRA2RL2
- Synonyms:
- ADRARL2
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-19
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- Lidocaine, a widely used local anesthetic, has been reported to exert anti-cancer activity against hepatocellular carcinoma (HCC). However, its molecular mechanisms remain incompletely understood. This study sought to elucidate the mechanisms underlying lidocaine’s effects on HCC. Potential lidocaine targets in HepG2 cells were identified using network pharmacology and transcriptomic profiling. The prognostic and clinical relevance of candidate genes were assessed through bioinformatics analyses. Key targets were validated by RT–qPCR. The functional role of SLC6A3 in regulating HepG2 cell proliferation, apoptosis, migration, and invasion was examined through in vitro assays. Network pharmacology predicted 433 lidocaine targets, while transcriptomic profiling revealed 442 differentially expressed genes. Nine overlapping targets (SLC6A3, CHRNB2, GRIN1, ADRA2C, LIPE, SLC18A2, KCNQ2, TERT, and ALOX12) were enriched in pathways associated with neuronal signaling, synaptic transmission, and drug addiction. Among these, SLC6A3 and TERT were significantly associated with poor prognosis and increased tumor immune infiltration. Both genes demonstrated predictive value for 1- to 2-year survival, with SLC6A3 showing the stronger prognostic relevance. Molecular docking revealed hydrophobic interactions between lidocaine and SLC6A3 (binding energy: −5.6 kcal/mol). Silencing of SLC6A3 markedly promoted apoptosis and suppressed proliferation, migration, and invasion of HepG2 cells. Collectively, these findings suggest that lidocaine inhibits HCC progression by targeting and downregulating SLC6A3. Lidocaine exerts anti-HCC effects by directly targeting and downregulating SLC6A3, thereby inducing apoptosis and suppressing tumor progression. - Source: PubMed
Publication date: 2026/04/07
Li PeiyangTong WulanHe HongLiu HaoYang Xi - Drug-induced amnesia is underrecognized due to absence of label indications. This study utilized the FAERS database to identify drugs associated with amnesia and investigated causal relationships through Mendelian randomization (MR) analysis. - Source: PubMed
Publication date: 2026/03/17
Li ChenChen YanYao YinhuiShang Yazhen - This study aimed to integrate bioinformatics, network pharmacology, and single-cell sequencing to explore the potential neuro-immune mechanisms by which the traditional Chinese medicine formula Xiao-Yao-San (XYS) ameliorates chronic stress-induced colorectal cancer (CRC) progression. - Source: PubMed
Publication date: 2026/03/03
Li YingYang ShengyaLi HaoranLi HuachaoSun YunchuanHe XinyingZhang YingruWang Yan - Diethyl phthalate (DEP) is a ubiquitous environmental endocrine-disrupting chemical (EDC). Epidemiological studies have suggested a potential association between DEP exposure and an increased risk of endometrial cancer (EC); however, its underlying molecular mechanisms remain largely unclear. Four GEO datasets were integrated, and differential expression analysis combined with weighted gene co-expression network analysis (WGCNA) was performed to identify candidate genes potentially linking DEP exposure to EC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore relevant signaling pathways. Machine learning models, coupled with Shapley Additive Explanations (SHAP), were employed to prioritize key genes. Molecular docking and molecular dynamics (MD) simulations were used to assess the binding affinity between DEP and the identified targets. A series of in vitro experiments in EC cell lines were subsequently conducted to validate the biological effects of DEP. Nineteen overlapping DEP-EC genes were identified, predominantly enriched in the MAPK, cAMP, and cGMP-PKG signaling pathways. Among them, FOS, NR4A1, ADRA2C, JUN, and SLC6A2 were prioritized as core genes through machine learning and SHAP analysis. Molecular simulations confirmed stable binding between DEP and these targets. In vitro assays demonstrated that DEP exposure induces oxidative stress, significantly enhances ERK1/2 and AKT phosphorylation, upregulates Cyclin D1/CDK4 expression, promotes G1/S phase transition, and facilitates EC cell proliferation. These findings suggest that DEP may promote endometrial carcinogenesis by triggering oxidative stress-mediated signaling crosstalk and accelerating cell cycle progression. This study establishes a multi-layered methodological framework-from computational screening and machine learning to experimental validation-offering novel mechanistic insights into the carcinogenic potential of environmental endocrine disruptors such as DEP. - Source: PubMed
Publication date: 2026/02/10
Chen XiWang ZijingWang FengfengWu YuexiaoHu DanCheng YuemeiXing YijuanDu JunhongJiang TaoYang YongxiuLiang XiaoleiBi Xuehan - This study investigates the regulatory role of microRNAs (miRNAs) in suppressing the overexpression of genes associated with Attention-Deficit Hyperactivity Disorder (ADHD), a genetically influenced neurodevelopmental disorder. A computational framework based on the 7mer-m8 seed match model was used to predict miRNA interactions with nine upregulated genes, aiming to identify miRNAs capable of binding to their coding sequences (CDS) and regulating gene expression. - Source: PubMed
Publication date: 2025/12/12
Roy BipashaBharadaj StellaBharadaj Srinjay KumarSharma DeepikaChakraborty Supriyo