Rabbit Endothelin 1,ET-1 ELISA Kit
- Known as:
- Rabbit Endothelin 1,ET-1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0067Rb
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Btlab
- Gene target:
- Rabbit Endothelin 1 ET-1 ELISA Kit
Related genes to: Rabbit Endothelin 1,ET-1 ELISA Kit
- Gene:
- BTF3P10 NIH gene
- Name:
- basic transcription factor 3 pseudogene 10
- Previous symbol:
- RAET1J
- Synonyms:
- -
- Chromosome:
- 6q25.1
- Locus Type:
- pseudogene
- Date approved:
- 2010-06-18
- Date modifiied:
- 2014-11-19
- Gene:
- EDN1 NIH gene
- Name:
- endothelin 1
- Previous symbol:
- -
- Synonyms:
- ET1
- Chromosome:
- 6p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-06
- Date modifiied:
- 2015-08-25
- Gene:
- ETM1 NIH gene
- Name:
- essential tremor 1
- Previous symbol:
- -
- Synonyms:
- FET1
- Chromosome:
- 3q13
- Locus Type:
- phenotype only
- Date approved:
- 1997-12-05
- Date modifiied:
- 2011-02-14
- Gene:
- GATB NIH gene
- Name:
- glutamyl-tRNA amidotransferase subunit B
- Previous symbol:
- PET112L, PET112
- Synonyms:
- -
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-03
- Date modifiied:
- 2016-06-21
- Gene:
- GFRA1 NIH gene
- Name:
- GDNF family receptor alpha 1
- Previous symbol:
- GDNFRA
- Synonyms:
- RETL1, GDNFR, GFR-ALPHA-1, RET1L, TRNR1
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-17
- Date modifiied:
- 2016-10-05
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- Previous genome-wide association studies have identified more than 400 prostate cancer (PCa) susceptibility loci. However, the tissue and spatial epithelial contexts through which inherited PCa risk may operate in the normal prostate remain incompletely understood. We analyzed normal human prostate spatial transcriptomic data using a gsMap-based framework to localize PCa association signals across spatially resolved prostate compartments. Spatial spots were clustered using SpaGCN and then manually curated and annotated based on matched histological images and canonical prostate marker gene expression. Because individual spatial spots may contain multiple cells, annotations were interpreted as compartment-enriched dominants rather than pure cell-type identities. PCa genetic association scores were aggregated within annotated compartments using Cauchy-combined p value and median spot-level p value as a complementary descriptive summary. Gene-level spatial correspondence was further assessed using Pearson correlation coefficients (PCCs) between gene-expression patterns and spot-level PCa gsMap signal. We annotated normal prostate tissue into four major compartments: basal epithelium-enriched, luminal epithelium-enriched, smooth muscle-enriched, and fibroblast stroma-enriched compartments. Basal epithelium-enriched compartments showed the strongest and most consistent enrichment for PCa association, with a Cauchy-combined p of 1.85 × 10 and a median spot-level based p of 3.67 × 10. Luminal epithelium-enriched compartments also showed strong enrichment, with a Cauchy p of 3.79 × 10 and a median-based p of 1.45 × 10. In contrast, fibroblast stroma-enriched compartments showed no evidence of enrichment (Cauchy p = 0.52; median p = 0.42), while smooth muscle-enriched compartments showed only modest evidence in the Cauchy-based analysis that was accompanied by a weaker median spot-level association signal (Cauchy p = 8.95 × 10; median p = 0.18). PCC analysis showed that genes with the strongest spatial correspondence to PCa gsMap signal were predominantly epithelial-associated, including CDH1, VAMP8, GMNN, TSPAN1, and FOXA1. In normal human prostate tissue, inherited PCa association localizes preferentially to basal epithelium-enriched and luminal epithelial-enriched compartments rather than to smooth muscle-enriched or fibroblast stroma-enriched compartments. Gene-level PCC patterns further support spatial alignment between PCa-associated gsMap signal and epithelial transcriptional programs. These findings provide proof-of-concept evidence for the spatial localization of inherited PCa susceptibility through the integration of large-scale population-based genetic data and spatial transcriptomics. - Source: PubMed
Publication date: 2026/08/30
Liu ShuaiChan Owen T MZhong HuaShahabi AliWu LangZhu Jingjing - Therapy resistance in prostate cancer arises from coordinated remodeling of malignant and stromal compartments, yet the mechanisms orchestrating this ecosystem adaptation remain elusive. Here, single-cell RNA sequencing of longitudinal biopsies obtained before and after androgen-deprivation therapy (ADT) delineated a therapy-induced stromal lineage bifurcation toward APOD and DPT fibroblast states. DPT fibroblasts activated a C3-ITGAX/ITGB2 complement signaling axis targeting macrophages, coinciding with suppression of M1 inflammatory programs, amplification of immune-checkpoint signaling, and a shift of CD8 T cells from cytotoxic to exhausted phenotypes. Concomitantly, we identified pre-existing malignant epithelial subpopulations characterized by reduced AR/KLK3 activity and heightened chromosomal instability that preferentially persisted following therapy. Integrative multi-omic analyses nominated TSPAN1 as a functional effector of castrate resistant prostate cancer (CRPC) and NRXN1 as a regulator of neuroendocrine plasticity through calcium-dependent signaling programs. Genetic silencing of either gene suppressed proliferation, clonogenicity, migration, and tumor growth, while attenuating neuroendocrine features in vitro and in vivo. Spatial mapping, functional perturbation, and stromal-epithelial co-culture experiments mechanistically established a therapy-induced DPT fibroblast-complement circuit that enforced immune evasion and channels epithelial trajectories toward CRPC or neuroendocrine prostate cancer. Collectively, these findings defined the DPT-complement-macrophage axis as an actionable vulnerability and position TSPAN1 and NRXN1 as therapeutic entry points to disrupt ADT-driven tumor ecosystem remodeling in prostate cancer. - Source: PubMed
Publication date: 2026/07/17
Chen YangDong DandanLiao JinlingLiao NaikaiLiu MengqiZhang QinChen SitingLiu QiLu YingLi TianyuZou ChunlinSong QiongWang QiuyanLiang JianXie QijiLi ChengyangWang MengyunCheng JiwenMo ZengnanWei Gong-Hong - Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy in which liver metastasis represents the principal determinant of poor prognosis. Although metastatic dissemination is thought to be driven by highly plastic tumor cells, the transcriptional features of liver metastasis-related initial cell (LMIC) and its spatial crosstalk with the metastatic microenvironment during PDAC progression remain incompletely defined. - Source: PubMed
Publication date: 2026/06/16
Li YangLiu Ya-DieJiang Zhi-YingLu Hong-Xiang - Benign prostatic hyperplasia (BPH) is a prevalent disease in elderly men. However, the plasma proteomic signatures for incident BPH are absent, hindering early prediction and risk stratification. We aimed to identify plasma proteins associated with incident BPH and the implicated biological pathways. - Source: PubMed
Publication date: 2026/06/12
Li HaoZhang YangchangChen LiYuan JiuhongQin FengWang XiandingXiong Yang - Tris (2-chloroethyl) phosphate (TCEP) is a widely used organophosphate flame retardant found in consumer products and human tissues. It is listed as a chemical known to cause cancer, but its effects on prostate cancer (PCa) progression remain unexplored. This study investigates the impact of TCEP on prostate tumor aggressiveness through comprehensive in vitro, in vivo, and multi-omics approaches. PCa cell lines (DU-145 and LNCaP) were treated with 1 or 10 μM TCEP to assess changes in migration, invasion, and proliferation. Male mice bearing PCa xenografts received daily intraperitoneal TCEP (100 μg/kg) to evaluate tumor growth and metastatic spread. Proteomic analysis of TCEP-exposed cells was performed to identify dysregulated pathways, followed by integration with patient transcriptomic data (The Cancer Genome Atlas-Prostate Adenocarcinoma, TCGA-PRAD) to derive a prognostic gene signature. Single-cell RNA-seq data (GSE176031) were analyzed to localize the expression of signature genes in tumor microenvironment compartments. Molecular docking simulations were conducted to assess the predicted structural compatibility between TCEP and candidate target proteins. TCEP exposure significantly increased PCa cell migration, invasion, and proliferation in vitro, and accelerated tumor growth and metastasis in vivo compared to controls. Proteomic profiling revealed that TCEP dysregulates pathways involved in cholesterol metabolism, lysosome function, and PPAR signaling. Mapping TCEP-altered proteins to TCGA data identified a four-gene signature (APOE, SPC25, TSPAN1, VGF) associated with shorter biochemical recurrence-free survival (P < 0.05). Single-cell analysis indicated that these genes are predominantly expressed in immune and stromal cells of the tumor microenvironment. Molecular docking simulations suggested potential structural compatibility between TCEP and the four protein targets, supporting possible molecular interactions that require further experimental validation. This study provides the first evidence that exposure to TCEP can drive PCa progression and metastasis. Our multi-faceted findings reveal novel mechanisms linking an environmental contaminant to PCa aggressiveness and uncover a four-gene prognostic biomarker signature, underscoring the impact of environmental toxicants on cancer progression. - Source: PubMed
Publication date: 2026/05/04
Li Xin-YangWang Zi-MingHu Si-YuanSun Jia-Chun