Proteins CD5L , Human
- Known as:
- Proteins CD5L , Human
- Catalog number:
- C580
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CD5L Human
Related genes to: Proteins CD5L , Human
- 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: Proteins CD5L , Human
Related articles to: Proteins CD5L , Human
- 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 - Bovine immunoglobulin M (IgM) from serum and colostrum has got considerable attention due to its immunological property against certain human pathogens. N-glycosylation being a key structural modification of IgM wherein glycan diversity exhibits significant role in maintaining its structural integrity and also bio functionalities; glycan heterogeneity in bovine serum and colostrum IgM complexes have not been explored till date. In this study, we have evaluated site-specific glycan heterogeneity of both commercially available bovine serum IgM as well as secretory IgM (sIgM) complex that was purified from bovine colostrum through the generation of N-glycopeptides followed by UHPLC-MS/MS analysis. N-glycosylation sites- N91ST, N260VS, and N307IS in μ heavy chain constant region (IGHM) displayed bi- and tri-antennary complex glycans with varying degree of core fucosylation and sialyation. While N329DT contained mainly oligomannose as well as hybrid glycans, only oligomannose types were present at N490VS. Both N307IS and N490VS indicated differential glycosylation. Glycans of joining chain (JC) were of bi-antennary complex glycans in both serum and colostrum IgM complexes. Glycans processing at individual sites of IGHM and JC were found in part similar to human counterparts yet bovine-specific glycan heterogeneity was observed. Secretory component (SC) of colostrum sIgM revealed mainly LacdiNAc containing bi-antennary complex glycans that differed substantially from human SC containing only LacNAc complex types with both core and terminal fucsoylation. Interestingly, CD5L was found associated with both serum and colostrum IgM complexes. Thus, the insights obtained in the study would form the basis for extended applications of bovine IgM complexes. - Source: PubMed
Publication date: 2026/05/17
Marihonnaiah SudarshanShivappa Gnanesh Kumar Belur - Ischemia-induced retinopathy is a defining feature of prevalent ocular conditions, including diabetic retinopathy and central retinal artery or vein occlusion. Therapeutic interventions for ischemic retinopathies show limited efficacy and adverse effects, highlighting the need to thoroughly investigate the underlying mechanisms. Histone deacetylase 3 (HDAC3), a member of the histone deacetylase family, plays a central role in regulating gene expression in myeloid cells (microglia and macrophages). We recently showed that myeloid HDAC3 deletion promotes tissue repair and functional recovery after retinal ischemia-reperfusion (IR) injury via efferocytosis, a process by which myeloid cells engulf and clear apoptotic cells. Here, we investigated the mechanism by which myeloid HDAC3 deletion enhances efferocytosis. Employing an in vitro efferocytosis assay coupled with RNA sequencing on HDAC3 KO macrophages revealed that the secreted protein, CD5 molecule-like (CD5L), was the most upregulated among other pro-efferocytic genes. In vivo, we found that CD5L levels markedly increased in the retinas of myeloid HDAC3 KO mice subjected to IR injury, and its expression colocalized with myeloid cells. Co-immunoprecipitation experiments showed that HDAC3 represses CD5L expression in a liver X receptor (LXRα)-dependent manner. Additionally, we found that CD36, a receptor for CD5L that facilitates the clearance of apoptotic cells, was upregulated in retinal myeloid cells after IR. In vitro, CD5L treatment enhanced efferocytosis via CD36. We then evaluated the role of CD5L in retinal IR injury using in vivo neuronal, vascular, structural, and functional endpoints. CD5L KO mice showed worsened outcomes after IR, whereas treatment with recombinant CD5L was protective against retinal ischemic injury. Collectively, our findings suggest that deleting HDAC3 enhances macrophage efferocytosis by upregulating the CD5L/CD36 axis. CD5L may serve as a promising therapeutic target to improve outcomes in ischemic retinopathy. - Source: PubMed
Publication date: 2026/04/20
Shahror Rami AZaman BushraChuesiang PiyananWild MelissaShosha EsraaLeung Yuet-KinMu ShengyuRusch Nancy JFouda Abdelrahman Y