Polyclonal ADAM10 (CT)
- Known as:
- Polyclonal ADAM10 (CT)
- Catalog number:
- pc-047
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal ADAM10 ()
Related genes to: Polyclonal ADAM10 (CT)
- 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: Polyclonal ADAM10 (CT)
Related articles to: Polyclonal ADAM10 (CT)
- Alzheimer's disease (AD) associated with insulin resistance represents a major challenge in sporadic neurodegeneration, where impaired neuronal survival and synaptic plasticity are compounded by aberrant DNA methylation. Epigenetic silencing of Wnt pathway genes under insulin-resistant conditions exacerbates β-amyloid accumulation, tau hyperphosphorylation, and oxidative stress. The present study aimed to establish insulin-resistant AD models and evaluate the mechanistic potential of DNA methyltransferase (DNMT) inhibition, with a specific focus on canonical Wnt/β-catenin restoration. An in vitro AD model was generated by exposing SHSY-5Y cells to streptozotocin (STZ, 400 μM), resulting in elevated DNMT1, Aβ, and sFRP1 levels, alongside reduced β-catenin and survivin expression. Treatment with the DNMT1 inhibitor 5-azacytidine (5-AZA), employed here as a mechanistic probe rather than a therapeutic candidate, reversed these changes, restoring Wnt signaling and attenuating amyloid burden. In vivo, intracerebroventricular administration of STZ (3 mg/kg) in rats induced an insulin-resistant AD-like pathology characterized by cognitive decline, increased pTau and acetylcholinesterase activity, and reduced neuroprotective markers. 5-AZA treatment improved memory and behavior, decreased pTau and AChE levels, and enhanced ADAM10, TREM2, BDNF, and antioxidant activity. Histological analysis further revealed preservation of neuronal layers and structural integrity. Collectively, these findings demonstrate that DNMT inhibition, exemplified by 5-AZA as a mechanistic tool, can mitigate STZ-induced molecular and behavioral alterations by relieving hypermethylation-mediated repression and supporting partial reactivation of canonical Wnt/β-catenin signaling. While 5-AZA itself is not a viable therapeutic option, the results highlight DNMT inhibition as a promising disease-modifying strategy in insulin resistance-associated AD. - Source: PubMed
Publication date: 2026/06/22
Paliwal ShivangiBhardwaj Jayant SinghTaliyan Rajeev - Alzheimer's disease (AD) is increasingly recognized as a systemic disorder, with skeletal muscle dysfunction contributing substantially to frailty and functional decline. Although amyloid-β (Aβ) has been detected in peripheral tissues, including skeletal muscle, how it drives muscle degeneration and whether exercise can counteract this process remain to be elucidated. - Source: PubMed
Publication date: 2026/06/21
Yang Ling-LingLuo Ya-XiSong DanLiu NaGong Li-HuanHeng TianZhou Xiao-HanLi Ya-XingChen Jia-HuiSong Zheng-XiLi YangWang Yu-LeBai Chuan-ChuanHe RuiHu PengZhou YangJia Gong-WeiYao Xiu-Qing - Lymphangiogenesis is essential for tumor lymphatic metastasis, yet the molecular mechanisms governing the activation of its key cytokine, VEGF-C, remain unclear. Herein, we identified a circRNA, circFOCAD, through VEGF-C maturation-associated multiple transcription sequencing. CircFOCAD is overexpressed in lymph node (LN)-metastatic bladder cancer (BCa) and is associated with poor prognosis. In footpad popliteal LN metastasis and orthotopic BCa models, circFOCAD enhances VEGF-C-dependent lymphangiogenesis and LN metastasis in BCa. Mechanistically, circFOCAD potentiates pro-VEGF-C cleavage by facilitating the expression of CCBE1 and its newly identified partner, the metalloprotease ADAM10. Specifically, circFOCAD promotes ADAM10 promoter H3K9 acetylation by recruiting YBX1. ADAM10 requires CCBE1 as a scaffold, binding at residue R301/R302, to interact with N-terminal propeptide of pro-VEGF-C at residue E58, provoking VEGF-C maturation and sustaining lymphangiogenesis in BCa. Clinically, neutralizing antibodies against CCBE1 and ADAM10 diminished the LN metastatic of BCa in a patient-derived xenograft (PDX) model. Our findings indicate that circFOCAD acts as an initiator of VEGF-C maturation and may represent a promising therapeutic target in LN metastatic BCa. - Source: PubMed
Publication date: 2026/06/18
Liu DaiyinPang MingruiLi YuanlongLiu ZhicongBi YifanZheng HanhaoLi WenjieLi PeixinAn MingjieChen JianchengLin YanJiang ChunPang JunHuang HuashengLin TianxinChen Changhao - High-grade gliomas (HGGs), particularly isocitrate dehydrogenase (IDH)-wild-type glioblastoma (GBM), remain highly lethal despite increasingly complex, tumor-intrinsic therapies. Converging evidence from models and human studies now positions neuronal activity as a core driver of glioma growth, invasion and epileptogenesis. This review synthesizes data on a mechanistically defined neuro-glioma circuit that links activity-dependent neuroligin-3 (NLGN3) shedding by the sheddase a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) ADAM10 with the formation and strengthening of neuron-glioma α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor synapses. Neuronal and oligodendroglial firing activates ADAM10, generating soluble NLGN3 (sNLGN3) that reprograms glioma cells toward a highly neural, synapse-competent state through kinase, epigenetic and mechanosensory pathways, including LYN proto-oncogene, Src family tyrosine kinase (LYN), phosphoinositide 3-kinase (PI3K)-mechanistic target of rapamycin (mTOR) and chondroitin sulfate proteoglycan 4 (CSPG4)-Piezo-type mechanosensitive ion channel component 1 (PIEZO1) signaling. Reprogrammed tumor cells then assemble calcium-permeable AMPA receptors and bona fide neuron-glioma synapses, receive excitatory input and propagate calcium waves across tumor networks, which in turn amplify peritumoral hyperexcitability and seizures, closing a positive feedback loop of activity-dependent growth. On this basis, we outline an "actionable circuit" spanning neuronal activity, NLGN3-ADAM10 shedding, intracellular signaling, synaptic integration and network remodeling, and we organize emerging pharmacologic and device-based strategies into a circuit-breaking framework that includes activity dampening, inhibition of NLGN3 shedding, blockade of downstream signaling and AMPA synapses, and network-level modulation. Finally, we highlight key translational challenges and opportunities in target selectivity, brain delivery, biomarker development and adaptive trial design, arguing that multidimensional, circuit-informed interventions may complement standard surgery, radiochemotherapy and molecular targeting in selected patients with activity-driven glioma. - Source: PubMed
Publication date: 2026/05/27
Tian Ya-FeiFan Jun-YueWu QiongPu Jun - Soluble receptor for advanced glycation end-products (sRAGE) and soluble Toll-like receptor 4 (sTLR4) are circulating pattern recognition receptor isoforms implicated in inflammatory regulation in type 2 diabetes mellitus (T2DM). This study examined the effects of supervised aerobic exercise training (AET) on circulating sRAGE, sTLR4, and related skeletal muscle inflammatory signalling outcomes in adults with T2DM. - Source: PubMed
Publication date: 2026/06/17
Perkins Ryan KMazo Corey EShadiow JamesVarshney PallaviMiranda Edwin RMiranda Victoria REisenberg MaggieNakamura Jane EOral Elif AHaus Jacob M