ADAMTS5
- Known as:
- ADAMTS5
- Catalog number:
- 001158A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAMTS5
Related genes to: ADAMTS5
- 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
Related products to: ADAMTS5
Related articles to: ADAMTS5
- Intra-articular triamcinolone acetonide (TA) injections are commonly used to manage joint synovitis despite reports that they accelerate cartilage degeneration. Previous studies found that TA minimally affected bovine cartilage, but effects in human cartilage remain unclear. - Source: PubMed
Publication date: 2026/04/21
Porter AnnieNguyen JuliePeng YingDiStefano StevenAsres NaodSnyder-Mackler LynnAxe MichaelLu X Lucas - Intervertebral disc degeneration (IVDD) is the primary pathological driver of chronic low back pain. While the mechanical role of skeletal muscle in spinal stability is well-established, its paracrine influence on IVDD-specifically via exosomes-remains poorly understood. This study investigated whether senescent skeletal muscle cell-derived exosomes (sSkM-Exos) aggravate metabolic dysregulation in nucleus pulposus cells (NPCs) and explored the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/16
Ma XiaoweiZhang WeiqiYin HanMiao DazhuangGao XiandaFu ChunxuChen WeiHou ZhiyongZhang QiZhang YingzeZhang Di - Temporomandibular joint osteoarthritis (TMJOA) is recognized as one of the most important oral-maxillofacial degenerative diseases, and affects a large group of the population worldwide. The progression of TMJOA is accompanied by an imbalance of cytokines in the joint cavity and a slow but long-lasting degradation of the joint tissues. FGF8, an important member of the fibroblast growth factor family, has been shown to be up-regulated in the cavities of osteoarthritis joints. However, its role in TMJOA progression remains unclear. Here, we established a mouse TMJOA model by using unilateral anterior crossbite (UAC), and investigated the role of FGF8 on the changes in condylar cartilage in the progress of TMJOA by using adeno-associated virus carrying FGF8 gene. We found that FGF8 accelerated the cartilage deterioration during TMJOA progression. FGF8 overexpression partially impaired the mature phenotype of chondrocytes by decreasing the expression of collagen type II (COL2A1) and aggrecan, and exacerbated chondrocyte hypertrophy by increasing the expression of collagen type X (COL10A1), matrix metallopeptidase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5). FGF8 promotes chondrocyte cytokine perturbation by up-regulating the expression profiles of inflammatory factors, chemotactic factors and interferons and down-regulating the expression of growth factors via the transcription factor JunB. Furthermore, FGF8-mediated JunB facilitates chondrocyte hypertrophy by binding to the promoters of Col10α1 and Mmp13. These results help understand the importance of FGF8 in the progression of TMJOA and provide cues for potential therapeutic strategies for osteoarthritis. - Source: PubMed
Publication date: 2026/04/15
Chen HaoranFeng ShuoLi ChengLiu YongtaoXue ChengXie JingZuo Tao - To investigate the regulatory role and molecular mechanisms of TSPAN9-mediated mitocytosis in an interleukin-1β (IL-1β)-induced rat chondrocyte senescence model, and to identify novel therapeutic targets for osteoarthritis (OA). - Source: PubMed
Chen QuanDa WaciliLuo NaijiaShen Bin - Focal damage to articular cartilage incurred during joint injuries frequently progresses to post-traumatic osteoarthritis (PTOA) due to the limited intrinsic repair capacity of cartilage. Chondrogenic progenitor cells (CPCs) residing within the cartilage can contribute to repair if effectively recruited and activated. Early interventions that enhance CPC homing and their subsequent chondrogenesis offer a regenerative strategy to prevent PTOA progression, addressing the current lack of effective early clinical therapies. GDF5 stands out as a key protein involved in cartilage development, yet its potential to mobilize CPC-mediated regeneration remains underexplored. - Source: PubMed
Publication date: 2026/04/14
He RuiGanesh VenkateswaranPhruttiwanichakun PornpojMartin James ASeol DongrimSalem Aliasger K