ADAMTS5 ELISA kit
- Known as:
- ADAMTS5 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAMTS5-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAMTS5 ELISA kit
Related genes to: ADAMTS5 ELISA kit
- Gene:
- ADAMTS5 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 5
- Previous symbol:
- -
- Synonyms:
- ADMP-2, ADAMTS11
- Chromosome:
- 21q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2015-11-09
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- To elucidate the molecular mechanism by which mechanical forces regulate aggrecan degradation in osteoarthritic cartilage. - Source: PubMed
Publication date: 2026/05/22
Lai Yen-YuChang Shu-Wei - ADAMTS5 cleaves chondroitin sulfate proteoglycans such as versican and aggrecan. Adamts5-/- mouse model exhibited aortic anomalies, and increased expression of Adamts4/5 led to excessive versican degradation and reduced cardiac jelly. In zebrafish, knockdown of adamts5 rescued the cardiac phenotype conferred by ccm1-deficiency in zebrafish embryos. Here, we generated an ADAMTS5 knockin mouse model (ADAMTS5KI) to characterize the effect of induced expression of human ADAMTS5 on the cardiovascular system in mice. Sustained expression of ADAMTS5 in the endothelium diminished cardiac jelly formation and proteoglycan deposition in the atrioventricular (AV) cushion and led to cardiac development arrest. Induced expression of ADAMTS5 in the endothelium of postnatal mice impaired cardiac valve patterning. Expression of ADAMTS5 in brain endothelial cells did not confer an obvious vascular defect. However, expression of ADAMTS5 in brain endothelial cells of Ccm2-deficient mice aggravated CCM lesion burden and shortened the life span of Ccm2-deficient mice. These findings suggest that tight regulation of ADAMTS5 in the endothelium is essential for cardiovascular development and structural integrity, and ADAMTS5 interacts with CCM signaling, contributing to CCM disease progression. - Source: PubMed
Publication date: 2026/05/18
Yang XiZhang JieyingDai ZifengYang TianziXie LiyaGao FeiZheng XiangjianHan Zhiming - Enhancer RNAs (eRNAs) play crucial roles in regulating cancer progression and serve as clinical biomarkers or therapeutic targets. However, systematic identification of oncogenic eRNAs and strategies to target them for precision oncology remain largely unexplored. In this study, we comprehensively identified tens of thousands of eRNAs significantly associated with cancer hallmark signatures across diverse tumor types, which we defined as hallmark eRNAs. These eRNAs exhibit a strong capacity to promote specific cancer hallmarks by mediating distinct oncogenic pathways in a cancer type-dependent manner. We also found that RNA-binding proteins can directly bind to eRNAs to regulate tumorigenesis. By integrating regulator-eRNA networks with drug response data, we identified drugs that target different cancer processes with specific associations to hallmark eRNAs. Specifically, in liver hepatocellular carcinoma, we characterized a hallmark eRNA, ADAMTS5e, which can activate the expression of oncogene ADAMTS5 to promote metastasis in vivo and in vitro. Cancer cells with high ADAMTS5e expression are resistant to sorafenib but are sensitive to the combination treatment of sorafenib and docetaxel, or sorafenib and navitoclax. Our study developed a platform to identify cancer-hallmark eRNAs and provided promising drug screening strategies. This approach was exemplified by the functional characterization of ADAMTS5e in cancer metastasis and the discovery of an effective combinational treatment. Together, these findings highlight the potential of hallmark eRNAs in precision oncology. - Source: PubMed
Publication date: 2026/05/15
Fu YongfengWang YunzheChai Zong-TaoZhang ChenyangFang YuzhuZhou JingqiGu XunWen BoZhang Zhao - Mechanical loading regulates chondrocyte health in articular cartilage. While physiological stimuli maintain homeostasis, supra-physiological stimuli from joint injuries disrupt it, leading to osteoarthritis (OA). OA progression involves complex mechanical and biochemical interactions across multiple length scales, which are challenging to investigate experimentally. In silico models provide an effective framework to explore these mechanisms. This study developed an integrated multiscale modeling framework for articular cartilage. It combined finite element (FE) models at tissue and cellular scales with an intracellular gene/protein regulatory network. The network incorporated key chondrocyte mechanotransduction and inflammatory pathways. It was implemented using a semi-quantitative formalism, capturing the directional and qualitative interplay between mechanical and inflammatory stimuli on chondrocyte biology, rather than quantitatively predicting absolute gene expression levels. A Hill's function was applied to link cellular forces from the FE model to a mechanical loading input to the regulatory network. Hill's function constants were calibrated through a genetic algorithm by matching simulated and experimental gene expressions of COL-II and ADAMTS5 in cartilage explants under 20% cyclic compression. As a validation step, model simulations were performed at 10% cyclic compression of cartilage explants. Predicted sGAG loss matched the trend of experimental data. COL-II and ACAN were overestimated and ADAMTS5 was underestimated compared with experimental data. These discrepancies are consistent with the semi-quantitative nature of the model and are attributed to the simplified representation of inflammation-dominated catabolic pathways at low mechanical loads in the current framework. Simulated chondrocyte responses at different locations revealed spatial heterogeneity in chondrocyte activity. Overall, the multiscale modeling workflow developed in this study represents a first step towards a powerful platform for mechanistically deciphering the complex interplay of mechanics and inflammation in articular cartilage across multiple length scales. - Source: PubMed
Publication date: 2026/05/12
Mukherjee SatanikLesage RaphaelleGeris Liesbet - Intervertebral disc degeneration (IVDD) is a major cause of low back pain, characterized by inflammatory responses and NLRP3 inflammasome-driven pyroptosis. Forsythiaside A (FTA), a primary bioactive compound derived from Forsythia suspensa, possesses anti-inflammatory, antioxidant, and anti-pyroptotic properties. However, its role in IVDD remains unclear. - Source: PubMed
Publication date: 2026/05/09
Xuan JunGao JianyuanWang XiangyangChen ChunhuiZhang Zhiguang