ADAM10 ELISA Kits for canine
- Known as:
- ADAM10 Enzyme-linked immunosorbent assay test Kits dog
- Catalog number:
- hadam10-elisa
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fivephoton
- Gene target:
- ADAM10 ELISA Kits for canine
Related genes to: ADAM10 ELISA Kits for canine
- 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 Kits for canine
Related articles to: ADAM10 ELISA Kits for canine
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia, with current therapies offering only limited symptomatic relief and lacking disease-modifying efficacy. Addressing this critical therapeutic gap, natural multi-target compounds like mulberroside A (MsA)-a bioactive glycoside from L.-present promising alternatives. This study investigated MsA's neuroprotective potential using scopolamine-induced AD-like mice and N2a/APP695swe cells. In vivo, MsA significantly ameliorated cognitive deficits and neuronal loss, concurrently enhancing cholinergic neurotransmission through increased acetylcholine levels and inhibited acetylcholinesterase (AChE)/butyrylcholinesterase (BChE) activities. MsA also upregulated neurotrophic factors (BDNF, CREB) in critical brain regions. In vitro, MsA restored cholinergic function, mitigated oxidative stress, and crucially reduced amyloid-β (Aβ) production by dual regulation of APP processing: promoting the non-amyloidogenic pathway via ADAM10 upregulation and inhibiting the amyloidogenic pathway via suppression of BACE1 and γ-secretase components. Mechanistically, these multi-target benefits were mediated by MsA's activation of the PI3K/AKT pathway, which triggered downstream inhibitory phosphorylation of GSK3β-directly reduced tau hyperphosphorylation-and activation of CREB/BDNF signaling. Collectively, our findings demonstrate that MsA confers comprehensive neuroprotection against AD pathology by simultaneously targeting cholinergic dysfunction, oxidative stress, Aβ accumulation, tau phosphorylation, and impaired neurotrophic signaling, highlighting its strong therapeutic candidacy. - Source: PubMed
Publication date: 2025/08/22
Li JinWang JiawenLi YaodongGuo JingyiJin ZiliangQiao ShourongZhang YunxiaLi GuoyinLiu HuazhenWu Changjing - Adult T-cell leukemia/lymphoma (ATL) is a malignant tumor of mature T lymphocytes induced by human T-cell leukemia virus 1, and it has a poor prognosis. Brentuximab vedotin (BV) is included in the treatment of CD30-positive ATL, but there are no predictive biomarkers for the treatment effects of BV. Serum soluble CD30 (sCD30) concentrations are increased in aggressive ATL at the time of diagnosis, but the effect of extracellular CD30 on BV-induced cell death in ATL is unknown. Similarly, a disintegrin and metalloproteinase 10 (ADAM10) and ADAM17 possess CD30 sheddase activity in anaplastic large cell lymphoma, but this activity is unclear in ATL. In this study, we showed that sCD30 concentrations were associated with BV activity in ATL-associated cell lines. Extracellular vesicles, such as exosomes containing CD30, also inhibited BV activity. Furthermore, knockdown of ADAM10/17 significantly reduced sCD30 concentrations and increased BV-induced cell death. These results suggest that ADAM10 and ADAM17 are involved in sCD30 production in ATL. Furthermore, endogenous extracellular CD30, such as sCD30 and CD30-positive extracellular vesicles shed by ADAM10/17, may be involved in BV-induced cell death. Taken together, our findings suggest that extracellular CD30 concentrations, including CD30 on extracellular vesicles, are a useful biomarker for BV therapy in ATL. - Source: PubMed
Sato KeisukeKozako TomohiroNakano AkiraKato NahoOgata KentaroKamimura HidetoshiSasaki HidenoriTakamatsu YasushiTakemoto ShigekiHonda Shin-Ichiro - Chemoresistance remains a major challenge in esophageal squamous cell carcinoma (ESCC) therapy, particularly resistance to 5-Fluorouracil (5-FU). This study uncovers how 5-FU resistance reprograms the tumour microenvironment, primarily through the up-regulation of ADAM10 and the release of soluble PD-L1, which collectively facilitate immune evasion. Using a 5-FU-resistant AKR mouse ESCC cell line (5-FU-AKR) and its parental counterpart, we applied third-generation DNA sequencing, proteomic analysis, and single-cell RNA sequencing to unravel the resistance-associated molecular and cellular shifts. We found that ADAM10 is significantly up-regulated in 5-FU-AKR cells, promoting soluble PD-L1 release, thereby limiting CD8+ T cell infiltration. Xenograft models further demonstrated enhanced tumourigenicity and immune exclusion in 5-FU-resistant tumours. These findings highlight a novel mechanism of immune suppression driven by ADAM10, suggesting that targeting the ADAM10-PD-L1 axis may restore anti-tumour immunity and improve treatment outcomes for 5-FU-resistant ESCC. - Source: PubMed
Publication date: 2025/09/16
Cai BangwuFeng XiaowenLuo ShujuanNurbahati AididarCui HongPeng TianyuanWang WeiLi HuifangLiu QingLu XiaomeiZheng Shutao - Reticulate acropigmentation of Kitamura (RAK) predominantly affects East Asian populations, though isolated cases and familial occurrences have been reported globally. Japanese researchers Kitamura et al. first described this condition in 1943. In 2013, pathogenic variants in ADAM10 (a disintegrin and metalloprotease 10) were identified as causative in multiple Japanese RAK pedigrees. The occurrence of RAK with Dowling-Degos disease (DDD) is relatively well-documented. However, rare associations with bilateral clinodactyly, nevus of Ito, dermatopathia pigmentosa reticularis, and progressive seborrheic keratosis have also been reported. RAK is an extremely rare autosomal dominant disorder. Café-au-lait macules (CALMs) represent common hyperpigmented lesions, yet no documented cases of RAK-CALMs coexistence exist in the literature to date. - Source: PubMed
Publication date: 2025/08/29
Gao BukuanWang HuijuanFan QianqianCong LinZhang GuoqiangLiu Xiaoye - Acute respiratory distress syndrome (ARDS) is characterized by excessive neutrophil recruitment, endothelial barrier dysfunction, and persistent inflammation. A Disintegrin and Metalloproteinase 10 (ADAM10) regulates leukocyte trafficking by cleaving adhesion molecules such as VE-cadherin and JAM-A, but its role in neutrophil-driven lung injury remains unclear. We investigated whether neutrophil-derived ADAM10 modulates neutrophil adhesion, migration, and pulmonary inflammation in a murine model of ARDS and assessed the effects of systemic ADAM10 inhibition. Using a neutrophil-specific ADAM10 knockout mouse model (ADAM10Catchup-Cre+) and pharmacological ADAM10 inhibition, we evaluated neutrophil recruitment, endothelial permeability, and adhesion molecule expression in lipopolysaccharide (LPS)-induced lung inflammation. Flow cytometry, immunofluorescence, and enzyme-linked immunosorbent assay (ELISA) were used to assess neutrophil migration, activation, and cytokine release. In vitro adhesion and transmigration assays were performed with human endothelial and epithelial monolayers using freshly isolated human neutrophils. Neutrophil-specific ADAM10 deletion did not affect endothelial permeability but reduced neutrophil recruitment into the alveolar space, associated with decreased CXCL1 and CXCL2/3 secretion and increased CD44 surface expression. ADAM10 inhibition enhanced adhesion but impaired transmigration, mirroring genetic deletion. Systemic inhibition also suppressed neutrophil activation and inflammatory cytokine release. Neutrophil ADAM10 promotes neutrophil migration and inflammation in ARDS by modulating chemokine signaling and adhesion molecule expression. Systemic ADAM10 inhibition reduces neutrophil infiltration and inflammatory cytokine production, suggesting ADAM10 as a potential therapeutic target to mitigate neutrophil-driven lung injury. - Source: PubMed
Publication date: 2025/09/12
Fuhr AnikaGoerlich MeikeBiedritzky AnnaKleinmaier CarolinHeck-Swain Ka-LinGamper-Tsigaras JuttaNgamsri Kristian-ChristosKonrad FranziskaKoeppen Michael