ADAMTS12 antibody
- Known as:
- ADAMTS12 (anti-)
- Catalog number:
- orb10043
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ADAMTS12 antibody
Related genes to: ADAMTS12 antibody
- Gene:
- ADAMTS12 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 12
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5p13.3-p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-05
- Date modifiied:
- 2018-02-13
Related products to: ADAMTS12 antibody
Related articles to: ADAMTS12 antibody
- Keloids are fibroproliferative scars that extend beyond the original wound margins and may cause pain, pruritus, and substantial psychosocial distress. Earlobe keloids are common, clinically distinctive lesions with high recurrence rates; however, the molecular mechanisms underlying their development remain incompletely characterized. Existing transcriptomic studies have largely focused on extracellular matrix genes, with limited integration of metabolism-related pathways. - Source: PubMed
Publication date: 2026/07/07
Tafner DanielleNaccarato Andressa MarangoniIsoldi Felipe ContoliFelix Gabriel de Almeida ArrudaNogueira Beatriz Ribeirode Morais Rafael Leite TavaresPesquero João BoscoGragnani Alfredo - Osteosarcoma (OS) suffers from stagnant survival rates due to high metastatic potential and genomic complexity. Here, we present a high-resolution single-cell transcriptomic atlas of the OS ecosystem using single-cell fixed RNA profiling (FLEX) of 40,401 cells across four clinical stages: treatment-naïve, post-chemotherapy, recurrent, and lung metastatic. We identified a metastasis-enriched malignant subpopulation, OB_3, characterized by aggressive transcriptional signatures and governed by which we validated as a prognostic marker for reduced overall survival. Functional experiments further demonstrated that silencing significantly reduced the migratory capacity of HOS and 143B OS cells and suppressed AKT and ERK phosphorylation, thereby supporting its role as an active driver of metastatic progression. Within the microenvironment, metastatic progression was defined by the emergence of RNASE1+ M2-like tumor-associated macrophages, an expansion of highly immunosuppressive S100A4+ regulatory T cells, and the specialization of PLVAP stalk endothelial cells driving tumor angiogenesis. Integrative interactome analysis revealed that these populations function as central coordinating hubs, utilizing MIF, SPP1, and Galectin signaling to orchestrate the metastatic niche. Our findings, validated across multiple external cohorts and tissue microarrays, delineate a coordinated multi-cellular network involving ADAMTS12+, RNASE1+, S100A4+, and PLVAP+ cells. This study clarifies how malignant and microenvironmental components co-evolve to facilitate systemic dissemination, providing a translational framework for precision risk stratification and the development of next-generation therapeutic strategies to counteract metastatic OS. - Source: PubMed
Publication date: 2026/06/26
Van Khanh NguyenDung Tran TrungHai HoangSang Nguyen Tran QuangThanh Tran DucQuang Dang MinhHa Nguyen ThiChi Nguyen Bui TamAnh Pham TuanDuc Pham MinhVan Bao TranHuyen Tran Dang AnhPhuong Vu ThiHien Ha Thi ThuPhuong Le ThiNhung Nguyen Thi HongKawada NorifumiThuy Le Thi Thanh - Liver fibrosis is not only a major cause of cirrhosis but also an important risk factor for hepatocellular carcinoma (HCC). Currently, few drugs can effectively reverse established liver fibrosis. FOXM1, a transcription factor aberrantly activated in chronic liver disease, has been implicated in fibrosis-associated hepatocarcinogenesis. Nevertheless, effective pharmacological strategies for targeting FOXM1 are still lacking. - Source: PubMed
Publication date: 2026/04/23
Wu DingyuDuan LeiTan DiHua XinyiLiang AnpingHuai RuipingQi ShanshanShang ZhixianJia ShijieQi HuiLiu XinrongZhao JielingJiang YuhongTan RuiMao Canquan - Osteosarcoma (OS) is an aggressive bone malignancy characterized by genomic instability and extensive extracellular matrix (ECM) remodeling. Members of the are matrix-associated proteases implicated in tumorigenesis; however, their roles in OS remain poorly defined. This study provides a comprehensive genomic, transcriptomic, and functional analysis of the ADAMTSs in OS, with particular focus on ADAMTS-3. Copy number alterations and mRNA expressions of ADAMTS genes were analyzed using the TCGA datasets. Gene set enrichment analysis and co-expression analyses identified biological processes associated with ADAMTS-3. Mechanistic studies investigated tumor necrosis factor-alpha (TNF-α) regulation of ADAMTS-3 in OS cells. Genomic profiling revealed frequent amplification and high mRNA expression of ADAMTS4, ADAMTS12, ADAMTS16, and ADAMTS17, indicating potential oncogenic activity. ADAMTS-3 was markedly overexpressed in OS tissues and cell lines, showing strong positive correlations with inflammatory (IL6, STAT3, NF-κB) and matrix-remodeling (MMP2, MMP9) genes. Functional enrichment indicated that ADAMTS-3 is associated with ECM organization, immune response regulation, and epithelial-mesenchymal transition. Mechanistically, TNF-α induced ADAMTS-3 transcription via activation of MEK, PI3K, JNK, and NF-κB pathways, with STAT3 and NF-κB by enhancing promoter activity. These findings identify ADAMTS-3 as an inflammation-responsive gene that links inflammatory signaling to ECM remodeling and tumor invasiveness in OS, representing a potential molecular bridge. - Source: PubMed
Publication date: 2026/05/03
Aymaz Ehed MuhammedAlper MeltemSav Feyza NurAydemir TuğşenKöçkar Feray - ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) family members, including ADAMTS-12, play a significant role in the breakdown of proteoglycans such as versican and neurocan. ADAMTS-12 -mediated degradation of neurocan could be relevant to neuronal plasticity, inflammatory responses, and neural tissue repair. Investigating this process may provide novel insights into the molecular mechanisms underlying neurodegenerative diseases, therefore contributing to the development of potential therapeutic strategies. The method for evaluating the neurocanase activity of ADAMTS-12 may offer a valuable tool for studying extracellular matrix remodeling in the central nervous system. The findings may contribute to the development of targeted therapies aimed at modulating the extracellular matrix integrity in neurological disorders and broaden our understanding of protease-substrate interactions in both physiological and pathological conditions. - Source: PubMed
Fontanil TaniaCal SantiagoObaya Alvaro J