Human MMP13 ELISA kit
- Known as:
- Human MMP13 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50677
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Human MMP13 ELISA kit
Related genes to: Human MMP13 ELISA kit
- Gene:
- MMP13 NIH gene
- Name:
- matrix metallopeptidase 13
- Previous symbol:
- -
- Synonyms:
- CLG3
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: Human MMP13 ELISA kit
Related articles to: Human MMP13 ELISA kit
- Patients with advanced breast cancer (BC) often experience bone metastasis, leading to severe skeletal complications and a significant decline in prognosis. However, the molecular mechanisms underlying BC bone metastasis remain largely unexplored. This study identified the long non-coding RNA LCAL4 as specifically upregulated in bone-metastatic BC, where it serves as an independent predictor of poor survival. Gain- and loss-of-function experiments in intracardiac and intratibial mouse models demonstrate that ectopic LCAL4 expression markedly enhances BC cell-mediated osteolytic bone metastasis. Mechanistically, LCAL4 acts as a molecular scaffold, directly binding the RNA/DNA-binding protein FUS, promoting its nuclear accumulation, and recruiting it to the MMP13 promoter. The LCAL4-FUS ribonucleoprotein complex then recruits RNA polymerase II and induces H3K4me3 deposition, thereby activating MMP13 transcription. Secreted MMP13 stimulates osteoclast differentiation and enhances bone-resorptive activity. The release of TGF-β from resorbed bone further accelerates tumor proliferation, establishing a self-reinforcing cycle that drives osteolytic metastasis. Notably, genetic disruption of the LCAL4-FUS-MMP13 pathway significantly suppresses BC bone metastasis. These findings highlight the pivotal role of the LCAL4-FUS-MMP13 axis in BC skeletal colonization and osteolytic progression, highlighting its potential as a therapeutic target for managing BC bone metastasis. - Source: PubMed
Publication date: 2026/06/18
Li QijiFan MingjianSun XiaotingYang XiaoyingZhang YuhaoZheng ZihanZhang XuanZhang XianZhu QingqingXiong ZhenchongLei KefengZhu ChengmingTian QinWang YunWang MengYe Liping - - Source: PubMed
Publication date: 2026/06/10
Takada KazuhideHayakawa SatoshiKomine-Aizawa Shihoko - Osteoarthritis (OA) is a widespread degenerative joint disorder marked by irreversible cartilage destruction. While signal transducer and activator of transcription 3 (STAT3) is recognised as a pivotal regulator in its pathogenesis, the downstream regulatory cascades of phosphorylated STAT3 (p-STAT3) in chondrocyte extracellular matrix (ECM) metabolism remain elusive. Our study sought to identify p-STAT3-mediated novel pathways driving OA. - Source: PubMed
Li PengfeiWong ChipiuWang YuqiangLiang TongzhouQue YichenGao WenjieLiu YilinGao Bo - This study investigated the effects of Aureusidin on extracellular matrix (ECM) degradation and pyroptosis of chondrocytes in osteoarthritis. Network pharmacology, molecular docking, and pull-down assays were initially conducted to explore the target of Aureusidin. Subsequently, Sprague-Dawley rats underwent anterior cruciate ligament transection (ACLT) received oral administration of Aureusidin. Cartilage damage was evaluated histopathologically by H&E and Safranin O-fast green staining. Primary rat chondrocytes were treated with Aureusidin under IL-1β stimulation. Pyroptotic morphology was observed under light microscopy. Propidium iodide staining and flow cytometry were conducted to evaluate membrane rupture. The expression of markers associated with ECM degradation and pyroptosis was analyzed by qRT-PCR, Western blot, immunohistochemistry, and ELISA. Caspase-3 was identified as a target for Aureusidin. Aureusidin (5, 10, 20 mg/kg) alleviated ACLT-induced cartilage damage and ECM degradation. It reduced the OARSI score and serum levels of CTX-II and COMP, while upregulating the expression of Col2a1 and Acan, and downregulating Adamts5, Mmp13, and Mmp3. Aureusidin also mitigated atypical pyroptosis, evidenced by inhibited expression of GSDME-N, Caspase-3, and Cleaved-Caspase-3, and decreased levels of IL-1β and IL-18. In IL-1β-stimulated primary chondrocytes, Aureusidin (5, 10, 20 μM) attenuated ECM degradation and Caspase-3/GSDME-mediated pyroptosis. Treating chondrocytes with the Caspase-3 inhibitor Z-DEVD-FMK under IL-1β-stimulated conditions alleviated ECM degradation and pyroptosis, but the additional application of Aureusidin did not provide further inhibition. Aureusidin has the potential to inhibit ECM degradation and Caspase-3/GSDME-mediated chondrocyte pyroptosis during osteoarthritis progression. Its therapeutic effects are dependent on binding to and modulating the Caspase-3. - Source: PubMed
Publication date: 2026/06/15
Feng ShangxiangSong KunZhang HaoWang ZhuoqunZhao YuchiZhao ZhongyuanWan Chao - Osteoarthritis (OA) joints present abnormal mechanical environments that limit drug retention and therapeutic efficacy. Current intra-articular systems cannot provide both sustained anti-inflammatory delivery and mechanical support. A celecoxib (CXB)-loaded "Nano-in-Nano" Hierarchical Delivery System (NiN-HDS) was developed to simultaneously optimize drug release and joint reinforcement. - Source: PubMed
Publication date: 2026/06/08
Yang ChuangzanHe HuashenLi YichaoHuang SaZhang YingnengXiao WeixinPeng ZhixuanLuo XueyuanJiang ShuohanLi YuCen LiranJia HuanhuanLiu YingBan Junfeng