CD59 Antibody
- Known as:
- CD59 Antibody
- Catalog number:
- csb-pa004947ea01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- CD59 Antibody
Related genes to: CD59 Antibody
- Gene:
- CD59 NIH gene
- Name:
- CD59 molecule (CD59 blood group)
- Previous symbol:
- MIC11, MIN1, MSK21, MIN2, MIN3
- Synonyms:
- 16.3A5, EJ16, EJ30, EL32, G344, p18-20
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD59 Antibody
Related articles to: CD59 Antibody
- Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and reversible depletion of targeted macrophage populations, and subsequent replenishment of RMs, followed by longitudinal scRNA-seq analysis of kidneys at baseline and days 1, 3, and 7 post-ablation. RM ablation triggered a rapid and sustained upregulation of , predominantly in proximal tubular epithelial cells (PTC1/PTC2), establishing a persistent chemotactic niche signal that coincided with macrophage repopulation. Regenerating RMs transitioned from inflammatory/stress-associated states toward metabolically active and proliferative phenotypes enriched in glycolysis, oxidative phosphorylation, MYC, and cell-cycle programs, with attenuation of canonical inflammatory pathways. Cell-cell communication analysis revealed an early burst of intercellular signaling at day 1, followed by progressive normalization, with fibronectin ), osteopontin (), chemokine (), and amyloid precursor protein () axes emerging as key mediators of niche restoration. Transcriptional network analysis identified a conserved regulatory module (, , , , , ) coordinating macrophage differentiation and regenerative programming, linking metabolic adaptation to lineage reconstitution. Sub-clustering revealed five dynamically shifting RM subsets with distinct inflammatory, remodeling, proliferative, and surveillance states, reflecting a hierarchical regeneration process. Functional validation using clodronate-mediated depletion in Secreted Phosphoprotein 1 (Opn)-deficient mice demonstrated impaired macrophage repopulation, establishing osteopontin as a critical regulator of RM regeneration. Together, these data define a coordinated epithelial-immune circuit in which Cx3cl1-driven chemotaxis, -dependent signaling, and a core transcriptional network orchestrate macrophage niche reconstitution and kidney repair following acute immune cell ablation. - Source: PubMed
Publication date: 2026/06/18
Islamuddin MohammadJi LixuanChen YilinSong KejingEllsworth Calder RRappaport JackWang ChenxiaoLiu ShumeiKolls JayXu XiaojiangQin Xuebin - Diabetic retinopathy and diabetic nephropathy are major microvascular complications of type 2 diabetes mellitus and may progress silently before clinical detection. Plasma glycated CD59 has been proposed as a marker linked to complement-mediated endothelial injury. This study assessed plasma glycated CD59 levels in type 2 diabetic patients with retinopathy, nephropathy, and combined microvascular complications. - Source: PubMed
Publication date: 2026/06/20
Chinta BhagatsinghKandimalla RameshAmbati Ranga Rao - COVID-19 has been closely associated with coagulation abnormalities. However, existing biomarkers, including D-dimer and fibrin degradation products (FDP), exhibit limited accuracy in stratifying disease severity and predicting long-term clinical outcomes. - Source: PubMed
Publication date: 2026/06/21
Zhou ZizhenLiu QiweiMa ShuangshuangShi AnkeTao YuzhiHu TianpengYan ShengtaoChen YinongJi XiaofanSun LuZhang HongSong WanluZhang ZhuYang PeiranZhai Zhenguo - CD59 is known as a membrane-bound regulator of the complement system that prevents the formation of the membrane attack complex on host cells. Here we report the metabolic consequences of CD59a knockout (KO) in mice fed a high-fat diet (HFD). Mice lacking CD59a were protected from the development of insulin resistance, glucose intolerance, hyperinsulinemia, obesity, and fatty liver. Mutants fed an HFD had elevated adiponectin levels and reduced leptin levels in plasma. Data from metabolic cages suggested decreased appetite and an increase in voluntary wheel activity in mutants. Liver transcriptome analysis showed a marked decrease of inflammatory and fibrotic pathways in CD59a KO mice on an HFD, and plasma and liver metabolomics were remarkably similar, indicating close correspondence between systemic and hepatic metabolic profiles. In conclusion, we uncover a noncanonical role of CD59a in the development of diet-induced insulin resistance, hyperinsulinemia, glucose intolerance, and obesity. - Source: PubMed
Publication date: 2026/06/17
Zeibak MarianKarbian NetanelRiahi YaelBaraghithy SajaAhmad LabibaTabib AdiAbromovitz IfatAgranovitz BellaBenyamini HadarGottlieb EyalTam JosephDor YuvalLeibowitz GilMevorach Dror - Schizophrenia pathogenesis may involve aberrant synaptic pruning mediated by excessive complement system activity (CSA) and altered microglial function. Microglia and CSA are tightly regulated by neuro-immune regulators (NIREGs) which regulate adverse innate response and play a critical role in the regulation of the synaptic pruning process. This study investigated transcriptional alterations of NIREGs in the brain and blood tissues of individuals living with schizophrenia (SZ individuals) vs. healthy controls (HC). - Source: PubMed
Publication date: 2026/06/11
Boughanmi Mohamed-ElMehdiLespine Louis-FerdinandLeboyer MarionDemily CarolineRey Romain