ADAMTS12 Antibody
- Known as:
- ADAMTS12 Antibody
- Catalog number:
- XW-8168
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- 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
- 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 - Decorin was identified as the most relevant biomarker in type 2 diabetes or obesity-related diseases, but its function in gestational obesity or gestational diabetes mellitus (GDM) remains unknown. RT-qPCR or western blot were employed to validate the expression of Decorin and ADAMTS12 in the umbilical cord blood or placental tissues of the aforementioned groups. Subsequently, an LPS + high glucose-induced primary trophoblast cell model was established to verify the expression of DCN and ADAMTS12 in trophoblasts. Based on this model, silencing (si) of Decorin, or Decorin recombinant protein (DCN-r) combined with si-ADAMTS12 intervention, was performed to investigate its effects on trophoblast cell proliferation, migration, invasion, and other characteristics. Compared to the normal pregnancy group, the levels of DCN and ADAMTS12 showed an increasing trend in the gestational obesity group and the GDM group. Notably, DCN and ADAMTS12 were markedly higher in the GDM with obesity group compared to either the gestational obesity or GDM-alone groups. LPS + high glucose inhibited the migration and invasion of primary trophoblast cells while promoting increased levels of DCN and ADAMTS12. Under LPS + high-glucose intervention, DCN-r further suppressed trophoblast cell migration and invasion while enhancing ADAMTS12 expression, whereas si-DCN reversed these effects. Additionally, si-ADAMTS12 attenuated the LPS + high glucose-induced decline in trophoblast cell migration and invasion and blocked the promoting effects of DCN recombinant protein. Silencing ADAMTS12 can inhibit the promotive effect of DCN on the migration and invasion capabilities of LPS + high glucose-induced primary trophoblast cells. Clinical trial number: not applicable. - Source: PubMed
Publication date: 2026/03/24
Chen QiulingHu TaoyanLuo Hui - - Source: PubMed
Publication date: 2026/03/06
Koch Lars