ADAM10
- Known as:
- ADAM10
- Catalog number:
- 001136A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAM10
Related genes to: ADAM10
- Gene:
- ADAM10 NIH gene
- Name:
- ADAM metallopeptidase domain 10
- Previous symbol:
- -
- Synonyms:
- kuz, MADM, HsT18717, CD156c
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-21
- Date modifiied:
- 2016-10-05
Related products to: ADAM10
Related articles to: ADAM10
- Diabetic kidney disease (DKD) is a common condition with few treatment options, and inflammation plays a pivotal role in its progression. Luteolin, a natural compound found in traditional Chinese herbs, is known for its anti-inflammatory properties, making it a potential treatment for DKD. But its effect and mechanisms in DKD remain incompletely elucidated. - Source: PubMed
Publication date: 2026/04/24
Deng LingchenWang YongShi ChunruWu JieYao JinShen WanjunZhang ZiyueLiu RanWang XuZhu HanyuZhang LiCai GuangyanZhou JianhuiHong QuanChen Xiangmei - LAG-3 is an inhibitory immune checkpoint implicated in T-cell dysfunction, but the significance of soluble LAG-3 (sLAG-3) in chronic hepatitis B (CHB) remains unclear. Whether checkpoint blockade can restore intrahepatic antiviral T-cell function during HBV antigen clearance also remains to be defined. - Source: PubMed
Publication date: 2026/04/21
Chen JingnaZu YingqiuJiang GeerFang ZhongYuan Zhenghong - Platelets, derived from megakaryocytes (MKs), are crucial for blood clotting. Identifying genes that regulate MK development and platelet production could advance treatments for blood disorders. We found that KxDL motif-containing 1 (Kxd1) knockout (KO) mice exhibited doubled platelet counts without impairment of individual platelet function. Kxd1-KO mice showed enhanced MK progenitor differentiation and rapid polyploid MK formation in vivo and in vitro. Mechanistically, KXD1 deficiency increased TSPAN14 levels by disrupting its endolysosomal trafficking, thus activating the ADAM10-Notch axis to drive MK polyploidization. In platelet/MK-specific Tspan14-KO mice, TSPAN14 deficiency impaired MK polyploidization and maturation. Our findings reveal that KXD1 is a key negative regulator of Notch signaling, controlling megakaryopoiesis mediated by TSPAN14. The KXD1-TSPAN14 axis is a promising therapeutic target for platelet disorders, including thrombocytopenia and myeloproliferative neoplasms, and as an interventional pathway for platelet production in transfusion medicine. - Source: PubMed
Publication date: 2026/04/16
Yuan YefengAi JiayiChen HanyuZhang PengLeng FeiGuo KaiQi ZhuangLiu KaifangZhang YingziLi TingYang LinNie FangyuanWei AihuaHao ChanjuanLi Wei - Proteases are common components of extracellular vesicles (EVs), yet the extent and functional relevance of ongoing proteolytic activity on EV surfaces remain largely unexplored. Such activity could significantly influence EV function and identity, with likely implications for EV-mediated signalling, recipient cell targeting, cargo delivery, and even translational applications ranging from biomarker discovery to therapeutic approaches. Here, we investigated the impact of sustained proteolysis on the composition of brain cell-derived EVs, focusing on A Disintegrin And Metalloprotease 10 (ADAM10), a key sheddase for signalling and adhesion proteins involved in neuronal and synaptic processes. Using primary rat cortical cultures, we found that numerous known ADAM10 substrates are part of small EVs (sEVs), and that their associated functions overlap with major sEV-mediated roles such as nervous system development, cell adhesion, and neurite outgrowth. Applying N-terminal proteomics to monitor sEV-derived cleavage fragments over time, we identified novel substrate candidates and demonstrated that sEV-associated ADAM10 activity remodels surface proteins involved in EV-cell interactions while generating soluble factors implicated in neuronal development. These findings suggest a previously unrecognised role for ADAM10 as a modulator of sEV composition and potentially cell-targeting specificity in the brain and position EVs as dynamic platforms for proteolytic processing 'on the move'. - Source: PubMed
Publication date: 2026/04/17
Reimann Christopher CAltmeppen Hermann CKoudelka TomasSchweizer MichaelaTholey AndreasMohammadi BehnamBär JuliaCheng LesleyGlatzel MarkusMikhaylova MarinaHill Andrew F - The pro-tumor function of mesenchymal stem cells (MSCs) in bladder cancer (BC) is not fully elucidated. This study integrates clinical cohorts, organoid models, and patient-derived xenografts (PDX) to dissect MSCs-derived TIMP1 as a key driver of BC progression. Using multiplex fluorescent immunohistochemistry and enzyme-linked immunosorbent assays, we found that elevated infiltration level of MSCs in BC tissues and TIMP1 levels in tissues/urine correlated with advanced tumor-stage, lymphovascular invasion, and reduced recurrence-free survival time, with MSCs infiltration positively associated with TIMP1 expression. Single-cell data analysis and mass spectrometry revealed TIMP1 as the predominant cytokine secreted by MSCs. Mechanistically, MSC-derived TIMP1 binds to ADAM10 to inhibit its extracellular shedding, thereby stabilizing cMet phosphorylation and activating the RAP1 signaling axis. Functional studies revealed that TIMP1 enhances intracellular Ca levels and VDAC1 expression through the RAP1 pathway, promoting the formation of vesicles derived from the inner mitochondrial membrane (VDIMs) to regulate mitochondrial quality control. Crucially, the TIMP1 inhibitor FXR agonist 3 suppressed MSCs-driven BC proliferation and attenuated tumor growth in PDX models by disrupting the cMet-RAP1 signaling pathway without systemic toxicity. Our findings propose targeting the MSCs-TIMP1-RAP1 axis as a novel therapeutic strategy for BC. - Source: PubMed
Publication date: 2026/03/17
Li PanYang EnguangZhang XinyuShi YiboChen ChaohuFan GuangruiWang YuhanWang HanzhangLiu NanZhou HongTian JunqiangCheng LiangDong ZhilongWang Zhiping