Human CD5 antigen-like,CD5L ELISA Kit
- Known as:
- Human CD5 antigenic-like,CD5L Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E3281Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Human CD5 antigen-like CD5L ELISA Kit
Ask about this productRelated genes to: Human CD5 antigen-like,CD5L ELISA Kit
- Gene:
- CD5L NIH gene
- Name:
- CD5 molecule like
- Previous symbol:
- API6
- Synonyms:
- Spalpha
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-11
- Date modifiied:
- 2015-11-30
Related products to: Human CD5 antigen-like,CD5L ELISA Kit
Related articles to: Human CD5 antigen-like,CD5L ELISA Kit
- Alzheimer's disease (AD), a neurodegenerative disorder, is the leading cause of dementia. Amyloid-beta (Aβ) and tau are major contributors to AD onset and progression. Here, we investigate the therapeutic potential of CD5L, a macrophage-specific secretory protein, in reducing Aβ accumulation and improving AD pathology. CD5L directly binds to Aβ, particularly the neurotoxic Aβ42, and blocks their aggregation. Moreover, CD5L enhances microglial phagocytosis against several forms of Aβ40 and Aβ42. In 5xFAD mice, a well-established AD murine model, forced expression of CD5L reduces Aβ plaque size and number. RNA sequencing shows that CD5L promotes phagocytic activity in microglia within the 5xFAD mouse brain. Furthermore, adeno-associated virus (AAV)-mediated delivery of CD5L improves cognitive function, as demonstrated by enhanced performance in the T-maze test. These findings highlight the role of CD5L in inhibiting Aβ aggregation and facilitating Aβ clearance via enhanced phagocytosis, offering a promising therapeutic strategy for AD. - Source: PubMed
Publication date: 2026/05/28
Maehara NatsumiHattori SatokoNakamura AkiraNagatoishi SatoruHirota AikaKudo KaiYoshikawa YuriMatsunaga RyoTsumoto KouheiMiyakawa TsuyoshiArai SatokoMiyazaki Toru - Small extracellular vesicles (sEVs) derived from mesenchymal stem cells represent a novel regenerative therapeutic strategy for various liver injuries. Menstrual blood-derived mesenchymal stem cells (MenSCs)-derived EVs may have therapeutic potential in treating liver fibrosis. In this study, systemically injected MenSCs-derived sEVs migrated into the injured liver, ameliorated serological indices, and decreased collagenous fiber accumulation in carbon tetrachloride (CCl)-induced liver fibrosis mouse models. We aimed to explore the underlying mechanism for the therapeutic effect of MenSC-sEVs. - Source: PubMed
Publication date: 2026/05/28
Chen LijunZhang NingHuang YuqiQu JingjingFang YangxinYuan YinFu JiaminWan DalongZhang QiChen LuWen ZuoshiChen XinYuan LiXu ZhenyuLi YifeiHu ChenxiaYan HuadongIzawa HiromiYoshimoto TakayukiLi LanjuanXiang Charlie - This prospective study evaluated first-trimester markers in pregnancies with isolated and combined forms of fetal growth disorders and gestational diabetes mellitus (GDM). Among 1869 screened women, the analysis included 83 controls, 55 GDM, 22 isolated intrauterine growth restriction (iIUGR), and 33 isolated large-for-gestational-age (iLGA) cases, with GDM subgroups stratified by fetal growth (GDM with normal fetal weight, GDM + IUGR, and GDM + LGA). First-trimester clinical and routine biochemical parameters were recorded, and serum concentrations of 80 proteins were measured using targeted LC-MRM-MS proteomics. Different trajectories emerged: IUGR phenotypes showed low PAPP-A/PlGF and high TSH ( < 0.01), indicating early placental insufficiency, while macrosomia showed opposite trends. GDM + IUGR represented the most severe "double hit" phenotype (lowest PlGF, earliest delivery), whereas GDM + LGA showed increased umbilical artery resistance despite excessive growth, suggesting endothelial dysfunction. Targeted proteomics revealed characteristic signatures: iIUGR featured low complement () and IGF proteins (, ) versus GDM and iLGA ( < 0.001); GDM + IUGR showed elevated and versus iIUGR ( < 0.05); GDM + LGA was marked by high and low , versus iLGA ( < 0.05). Complement and IGF pathways were consistently implicated. Machine learning achieved 77% sensitivity for IUGR prediction using clinical parameters and 88% sensitivity for LGA prediction using proteomic data. These findings demonstrate that fetal growth disorders represent pathophysiologically unique entities detectable in the first trimester, enabling early risk stratification and personalized management. - Source: PubMed
Publication date: 2026/05/08
Starodubtseva NataliaTokareva AlisaFrankevich NataliaKononikhin AlexeyBugrova AnnaIndeykina MariaKukaev EvgeniiDerenko AnnaFrankevich VladimirNikolaev EvgenySukhikh Gennady - Chronic hepatitis B and C remain major causes of progressive liver disease, while HBV-HCV coinfection is associated with accelerated fibrosis and hepatocellular injury. - Source: PubMed
Publication date: 2026/05/08
Dumitrache Păunescu AlinaIonescu Șuțan Nicoleta AncaSoare Liliana CristinaPonepal Maria CristinaȚânțu Ana CătălinaȚânțu Monica MarilenaBaniță Ileana MonicaPisoschi Cătălina Gabriela - Chronic kidney disease (CKD) encompasses multiple pathogenic mechanisms manifested by inflammation, fibrosis, oxidative stress and cell death. We previously showed that circulating protein CD5L (or AIM) ameliorates acute kidney injury, so we explored its effect in a mouse model of unilateral ureteral obstruction (UUO)-induced renal fibrosis. Here, we show a unique kidney-protective pathway mediated by CD5L. CD5L is endocytosed into renal epithelial cells, where it reduces oxidative stress, decreasing cell injury and death. This effect is supported by both a cysteine-dependent direct antioxidant activity of CD5L and enhancement of Nrf2-associated antioxidant responses. In addition, our data suggest that suppression of sphingomyelinase activity and reduction of cellular ceramide may contribute, at least in part, to CD5L-associated augmentation of Nrf2 nuclear transport. These effects depend on the reactive cysteine residue on the CD5L surface. Consistent with these findings, recombinant CD5L treatment in UUO mice reduces sphingomyelinase activity, activates Nrf2, and lowers oxidative stress, alleviating inflammation, fibrosis, and kidney injury. Our findings uncover a novel antioxidant pathway mediated by CD5L with potential implications for CKD-associated fibrotic mechanisms. - Source: PubMed
Publication date: 2026/05/23
Kudo KaiIkeda TakashiIkeda KazutakaMaehara NatsumiHirota AikaYoshikawa YuriMori HarukaTakayama MasumiYasuda KeisukeTezuka TetsushiTakagi ToshioArai SatokoMiyazaki Toru