ADAM10 ELISA kit
- Known as:
- ADAM10 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAM10-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAM10 ELISA kit
Related genes to: ADAM10 ELISA kit
- 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 ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: ADAM10 ELISA kit
- Angiotensin-converting enzyme 2 (ACE2) is a key regulator of the renin-angiotensin-aldosterone system (RAAS). It also acts as a receptor for SARS-CoV-2 and stabilises the B0AT1 amino acid transporter at the cell surface. Therefore, surface expression of ACE2 is crucial for these physiological processes. ACE2 is released as a soluble, catalytically active form, partly through ectodomain shedding. This process mainly involves the sheddases ADAM10 and ADAM17, but the exact regulatory mechanisms remain unclear. We assessed 11 naturally occurring single-point mutations in the ACE2 stalk region. Most variants showed significantly reduced release compared to wild-type (WT) ACE2; however, the single point mutations P734L and G726R significantly increased their release. ACE2_P734L also exhibits higher surface expression, directly increasing the surface levels of B0AT1. Despite B0AT1 and ACE2 forming a tight tetrameric complex, this did not affect ACE2 shedding. This suggests that complex formation does not restrict sheddase access. Overall, these data identify the ACE2 stalk region as a major determinant of shedding efficiency. Naturally occurring variants in this region can substantially affect the release of soluble ACE2, potentially contributing to interindividual differences that are relevant for pathophysiological processes. - Source: PubMed
Publication date: 2026/04/29
Wiersch FlorianLux ChristineVanderliek-Kox JuliaSchun KatharinaLudwig AndreasDüsterhöft Stefan - Alzheimer's disease (AD) remains an incurable disorder with severe clinical consequences. The type 3 diabetes hypothesis posits that AD may constitute a neuroendocrine disorder driven by disrupted insulin and insulin-like growth factor signaling. Amyloid pathogenesis in AD is characterized by the accumulation of beta-amyloid (Aβ) monomers, their subsequent oligomerization, and amyloid deposition. One of the causes of Aβ accumulation is disruption of amyloid precursor protein (APP) processing due to imbalance in ADAM10 and BACE1 expression. In recent years, increasing attention has been devoted to investigating the role of environmental factors in AD pathogenesis. The receptor for advanced glycation end products (RAGE) serves as a key molecular link between environmental exposure and neuroinflammatory pathology. Formaldehyde (FA) is one of the most widespread environmental pollutants. Its involvement in amyloid plaque formation has been previously reported; however, the molecular mechanisms underlying this process remain insufficiently understood. Moreover, most available data are based on prolonged FA exposure, whereas industrial FA emissions are often short-term. The objective of this study was to determine whether brief intranasal administration of FA, modeling episodic industrial pollution, induces RAGE-mediated neuroinflammation and amyloid deposition in CD1 mice. Mice received intranasal FA at environmentally relevant 0.02 mg/day or 0.2 mg/day doses for seven days; an additional group was co-treated with insulin. Cognitive function was assessed using passive avoidance (PA) and radial arm maze (RAM) tests, and synaptic plasticity was evaluated by electrophysiology. Hippocampal tissue was analyzed for RAGE expression, / gene balance, Aβ42 monomer levels, and amyloid deposits using optimized Thioflavin-S (Th-S) staining. We observed cognitive decline in mice receiving intranasal FA administration. Elevated blood glucose levels were also observed following intranasal FA exposure. Sustained impairment of glucose metabolism led to overexpression of the RAGE in the hippocampus. There was also an imbalance of ADAM10 and BACE1 expression in the hippocampus. This was caused by overexpression of RAGE, as the enhanced interaction of the ligand and RAGE is a key factor disrupting this balance. Finally, Th-S staining confirmed amyloid deposition in mice subjected to intranasal FA exposure. This study provides new insights into the RAGE-mediated mechanisms by which FA contributes to the pathogenesis of AD. - Source: PubMed
Publication date: 2026/03/30
Mikhailov Ilya GMikhailova Milana SBaklashov Alexey DPonamareva Polina SShumilova Sofya NShuvaev Andrey NBelozor Olga SShuvaev Anton N - Doxorubicin (Dox) is a potent first-line chemotherapeutic and widely administered against different types of cancer, but is associated with a myriad of side effects, including cancer/chemotherapy-associated thrombosis and drug-induced thrombocytopenia (DIT). Although we and others have reported Dox-induced platelet activation, the binding partner of Dox on platelets has not been previously explored. Here, we found human and mouse platelet aggregation triggered via C-Type Lectin-like Receptor-2 (CLEC-2) was obstructed by Dox, but aggregation induced by classical agonists like ADP, collagen/collagen-related peptide, or thrombin receptor-activating peptide 6 (TRAP6), was unaffected. By Isothermal Titration Calorimetry, we detected a high binding affinity between Dox and recombinant CLEC-2 at 4.2 ± 2.4 nM. Interestingly, we found significant GPIb⍺ shedding from human and mouse platelet surfaces following Dox treatment. Consistently, GPIb⍺ shedding was recapitulated following anti-CLEC-2 monoclonal antibody treatment. Using Piceatannol to selectively inhibit CLEC-2 intracellular signaling or the pan-Matrix Metalloproteinases (MMP) inhibitor GM6001 rescued GPIbα from both Dox and CLEC-2 mAb-induced shedding. Using GI254023X or GW280264X to specifically inhibit ADAM10 or ADAMs10/17, respectively, revealed inhibition of ADAM10/17, but not ADAM10 exclusively, prohibited GPIbα shedding. Collectively, this implicates the classical sheddase of GPIbα, ADAM17. Thus, we pinpointed CLEC-2 as a binding partner for Dox on platelets and a novel pathway of ADAM17-mediated GPIb⍺ shedding via CLEC-2. These data not only provide insights into a mechanism of Dox-induced platelet activation, thrombosis, and DIT, but also reveal putative precision therapeutic approaches for Dox-treated patients and nominate CLEC-2 inhibition as a means to regulate thrombotic disease and/or bleeding disorders. - Source: PubMed
Publication date: 2026/04/27
Rousseau ZackaryMa WenjingLong TianleSlavkovic SladjanaQiu XinLao XiaomeiWu Xun GraceJoshi KaishivZhu Yunqing AmeliaZhu GuenghengThu Kelsie LNi Heyu - 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: 2026/04/22
Chen JingnaZu YingqiuJiang GeerFang ZhongYuan Zhenghong