ADRA1D
- Known as:
- ADRA1D
- Catalog number:
- 001240A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADRA1D
Ask about this productRelated genes to: ADRA1D
- Gene:
- ADRA1D NIH gene
- Name:
- adrenoceptor alpha 1D
- Previous symbol:
- -
- Synonyms:
- ADRA1R, ADRA1A, ADRA1
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2014-11-19
Related products to: ADRA1D
Related articles to: ADRA1D
- Sea cucumbers () show fleeing, adhesion, and thanatosis patterns upon exposure to various stressors. However, the molecular mechanisms underlying these contrasting stress response patterns remain largely unknown. In the present study, we performed a transcriptomic analysis of coelomocytes on stressed sea cucumbers to elucidate the potential molecular mechanisms. The RNA-seq results revealed that several matrix metalloproteinase () family genes, along with , , and (which are involved in neuroactive ligand-receptor interactions), were significantly upregulated in the fleeing pattern. These genes may facilitate rapid movement. In the adhesion pattern, and were significantly downregulated, and the differentially expressed genes (DEGs) were significantly enriched in the longevity regulating pathway, accompanied by downregulation of and . These genes and the pathway may be involved in the reallocation of energy resources during the adhesion pattern. In the thanatosis pattern, DEGs were significantly enriched in the MAPK signaling pathway (including upregulation of and ) and in the Rap1 and Ras signaling pathways (with downregulation of key genes: , , and ). These genes potentially contribute to sustaining the thanatosis pattern. These transcriptomic profiles provide novel insights into the distinct molecular signatures underlying each stress response pattern in . - Source: PubMed
Publication date: 2026/06/22
Wu GuoWu HengyeWang XiajingGao QiangZhao Chong - Primary liver cancer (PLC) is a leading cause of global cancer mortality. Yangzheng Xiaoji Decoction (YZXJD), a traditional Chinese medicine based on "Fuzheng Xiaoji" principles, is used as adjunctive PLC therapy, yet its underlying molecular mechanisms require further characterization. - Source: PubMed
Publication date: 2026/06/15
Yang ShengboLiu RuiWen ShuaiWang YaTai NanTian Jie - BACKGROUND: The development and progression of bladder cancer are closely linked to its complex tumor microenvironment. Hedyotis diffusa and Scutellaria barbata (HD-SB) are commonly used as a prominent herbal pair for treating bladder cancer. However, the pharmacological targets and molecular mechanisms by which HD-SB impacts bladder cancer require further elucidation. Additionally, it remains uncertain whether this herbal pair affects the prognosis and treatment efficacy of bladder cancer. METHODS: We employed network pharmacology to predict the targets of HD-SB and bladder cancer, identifying overlaps with prognostic genes linked to the overall survival of bladder cancer patients in the TCGA dataset. Subsequently, we utilized least absolute shrinkage and selection operator (LASSO) and Cox regression analyses to pinpoint a prognostic signature and construct a prognostic model. We further explored the correlations between risk scores, immune cells, immune checkpoint genes, and treatment efficacy. Single-cell RNA-sequencing (scRNA-seq) was used to profile the expression of prognostic genes across various cell types, and immunohistochemistry validated the protein levels of these targets. Molecular docking studies were conducted to clarify the interactions between HD-SB components and the identified genes, and in vitro experiments demonstrated the effects of HD-SB on bladder cancer cells. RESULTS: Venn diagram analysis identified 497 common targets shared between HD-SB and bladder cancer. LASSO and Cox regression identified a 15-gene prognostic signature, including VEGFA, EGFR, MYC, PDGFRA, JUN, FN1, PTPN6, PTGER3, MAP2, CALM1, CTSV, CES1, ADRA1D, PYGL, and PLA2G1B. Kaplan-Meier analysis showed better overall survival in the low-risk group (median 19.8 months) versus the high-risk group (median 15.9 months). Linear regression analysis revealed a significant correlation between risk scores and specific immune cell types, as well as the dysregulated expression of immune checkpoint genes across different groups. The prognostic gene-based risk score was also found to correlate with the efficacy of both immunotherapy and chemotherapy. Six key targets—VEGFA, MYC, JUN, FN1, PTPN6, and CALM1—were validated through scRNA-seq and immunohistochemistry. Molecular docking analysis demonstrated that components of HD-SB bind with high affinity to these signature targets. In vitro experiments showed that HD-SB effectively inhibited bladder cancer cell viability, colony formation, and migration. CONCLUSION: This is the first study to explore the potential of HD-SB in enhancing the prognosis and treatment outcomes of bladder cancer through network pharmacology, bioinformatics, and experimental approaches. While the focus is primarily on tumor microenvironment-related factors, the findings provide valuable insights into the molecular mechanisms of HD-SB and identify potential novel targets for bladder cancer therapy. - Source: PubMed
Publication date: 2026/02/13
Liu YuanDuan LiyuanZhu MengweiZhou ZhenzhenZhao PinZhan YonghaoZhang XuepeiZhu Zhaowei - Irritable bowel syndrome (IBS) is a prevalent disorder whose most debilitating symptom is pain. The complex, multifactorial nature of IBS pain leads to highly variable and often inadequate responses to self-management, underscoring the urgent need for personalized prediction models. - Source: PubMed
Publication date: 2025/10/08
Chen JieLi AolanWu WeiziXu WanliZhao TingtingStarkweather Angela RRodriguez LeonelChen Ming-HuiCong Xiaomei S - Osthol (OST), a natural coumarin, exhibits anti-inflammatory and metabolism-regulating potential. This study investigated whether OST ameliorates obesity-associated metabolic dysregulation and inflammation by targeting ADRA1D-mediated T helper 17 (Th17) differentiation. High-fat diet (HFD)-induced obese mice were treated with OST. Metabolic parameters including body/organ weights, serum lipids, hepatic enzymes, and histopathology were assessed. Th17-related and inflammatory markers were evaluated via flow cytometry, ELISA, RT-qPCR, and Western blot. In vitro Th17 differentiation (primary murine CD4⁺ T cells) and lipid metabolism (3T3-L1 adipocytes) models were used. ADRA1D was identified as a key target via bioinformatics and validated through overexpression in cells and mice. OST significantly reduced HFD-induced weight gain, liver and fat mass, serum triglycerides (TG), free fatty acids (FFA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic lipid deposition, and adipocyte hypertrophy. OST suppressed Th17 differentiation, CD4⁺IL-17A⁺ and CD4⁺RORγt⁺ cell proportions, and pro-inflammatory cytokines (IL-17A, IL-6, TNF-α), while elevating anti-inflammatory cytokines (IL-10, TGF-β). OST downregulated IL-17RA, TRAF6, and Act1 expression and inhibited ERK1/2 and PI3K phosphorylation. In vitro studies confirmed the dose-dependent inhibitory effect of OST on Th17 polarization. Mechanistically, OST modulated Th17-related signaling via ADRA1D. ADRA1D overexpression partially reversed OST-mediated suppression of Th17 differentiation, expression of lipogenic genes (FASN, PPARγ), and lipid droplet accumulation. In vivo, ADRA1D overexpression attenuated the beneficial effects of OST on metabolic parameters and tissue inflammation, confirming ADRA1D dependence. OST ameliorates obesity-related metabolic dysregulation and inflammation by inhibiting ADRA1D-mediated Th17 differentiation, highlighting ADRA1D as a key mediator and potential therapeutic target for immunometabolic disorders. - Source: PubMed
Publication date: 2025/10/21
Li PeiHe ChaoWu ChaoZhou XinboMa YiranDeng Qi