CD59
- Known as:
- CD59
- Catalog number:
- 11-233-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD59
Related genes to: CD59
- 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
Related articles to: CD59
- Red blood cell (RBC)-camouflaged nanocarriers provide a biomimetic strategy to reduce immune clearance and improve tumour-directed drug delivery. Here, we engineered an RBC-camouflaged albumin nanoplatform co-loaded with oxaliplatin (Oxa) and zinc oxide nanoparticles (nZnO), termed C-Alb, for colorectal cancer therapy. The optimized formulation exhibited a uniform hydrodynamic size of 139.3 ± 2.5 nm, a zeta potential of -17.6 ± 2.3 mV, efficient Oxa/nZnO loading, good colloidal stability, and pH-responsive Oxa/Zn release, with enhanced release under acidic/reductive tumour-mimicking conditions. RBC membrane cloaking preserved vesicular morphology and key membrane-associated components, including glycoproteins, sialic acid, CD47, CD55, and CD59, while reducing macrophage uptake. In CT26 cells, C-Alb enhanced cytotoxicity (IC₅₀ = 4.27 μM), increased caspase 3/7 activation, and induced ICD-associated calreticulin exposure, ATP secretion, and HMGB1 release. These responses promoted M1 macrophage polarization, dendritic cells maturation, and macrophage-mediated phagocytosis of treated tumour cells. The formulation also downregulated CD44 and reduced CT26 adhesion and migration. In CT26 tumour-bearing mice, RBC coating prolonged systemic exposure, reduced RES-associated accumulation, enhanced tumour Oxa deposition, improved antitumour efficacy, and maintained acceptable systemic tolerability. Therefore, C-Alb integrates immune-evasive delivery, Oxa/nZnO co-delivery, ICD-associated immune activation, and improved in vivo antitumour performance. - Source: PubMed
Publication date: 2026/08/27
Hamdi MohamedAbdel-Bar Hend MohamedElmowafy EnasElKashlan Akram MMansour MaiAl-Jamal Khuloud TAwad Gehanne A S - Gliomas, particularly glioblastoma (GBM), are characterized by aggressive progression and profound immune evasion. The complement system which is a fundamental component of innate immunity comprising classical, alternative, and lectin activation pathways converging on target cell lysis, is frequently dysregulated within the tumor microenvironment, where it plays a pivotal role in promoting tumor survival and immune shielding. The complement system, often dysregulated in the tumor microenvironment, plays a pivotal role in these processes via regulators like Factor H (CFH), Factor I (CFI), and Clusterin (CLU). This systematic review analyzes their expression, regulation, and dual roles in immune shielding and oncogenic signaling. - Source: PubMed
Publication date: 2026/08/21
Alomari OmarAlomari TasneemGüney BeyzanurEyvazova HabibaBenamara Tesnim SoukainaAlomari SondosBingöl MerzanOdabas Hatice - Structural motifs can be conserved among proteins with low primary-sequence identity, potentially supporting distinct yet related molecular functions. Endogenous phospholipase A inhibitors from snake plasma (sbPLIs) include the γ-type inhibitor from Crotalus durissus terrificus, known as Crotalus neutralizing factor (CNF), which protects the snake by selectively inhibiting the lethal and PLA activities of crotoxin (CTx). CD59, a complement regulator and single-LU-domain member of the Ly6/uPAR superfamily, shares the three-finger fold with CNF, raising the possibility of structural and functional convergence. Here, CD59 linear peptide arrays produced by SPOT synthesis were probed with CB, the PLA subunit of CTx, to identify CD59 regions capable of binding CB. Two reactive clusters were mapped, and derived peptides were synthesized and tested for their ability to inhibit the PLA activity of CTx and CB in vitro. Four CD59-derived peptides interacted with CB on the arrays; however, none inhibited PLA activity, in contrast to native CNF used as a positive control. These findings indicate that, although CD59 contains linear segments that recognize CB, this interaction is not sufficient to reproduce the PLA-inhibitory function of CNF, suggesting that any functional interplay between these Ly6/uPAR proteins is likely to depend on more complex structural determinants. - Source: PubMed
Publication date: 2026/08/20
Fortes-Dias Consuelo LatorreOrtolani Paula LadeiraCampos Patrícia CotaSalvador Guilherme Henrique MarchiVillas Boas Isadora MariaAmaral de Melo LutianaSant'Ana Osvaldo AugustoTambourgi Denise VilarinhoFontes Marcos Roberto Mattos - Toxoplasma gondii (T. gondii) infection disrupts pregnancy by modulating decidual natural killer (dNK) cells function. This study investigates how T. gondii regulates CD59 expression in dNK cells and its impact on pregnancy outcomes. - Source: PubMed
Publication date: 2026/08/18
Wang ShuyanHuo LuyunZou YanYang RuohanWang XiaoZhang HaixiaRen LiqinYang JingLi JieHu XuemeiRen Yushan - Paroxysmal nocturnal haemoglobinuria (PNH) is a rare, acquired clonal haematopoietic stem cell disorder characterised by intravascular haemolysis, thrombosis and bone marrow failure. It results from an acquired somatic mutation in the X-linked phosphatidylinositol glycan Class A (PIGA) gene, leading to deficiency of glycosylphosphatidylinositol-anchored complement regulatory proteins, particularly CD55 and CD59, and uncontrolled complement-mediated haemolysis. Although sickle cell disease is the most prevalent haemolytic anaemia in Kenya, other aetiologies need to be considered. We describe a case series of seven patients with PNH confirmed by fluorescent aerolysin reagent (FLAER) flow cytometry. Patients were young, aged 17-38 years (median age of 23 years), with a predominance of males. All presented with recurrent symptomatic anaemia requiring multiple transfusions. One patient had pancytopenia due to very severe aplastic anaemia, while another presented with mesenteric vein thrombosis complicated by bowel ischaemia. All patients had large PNH clones on flow cytometry. Management was largely supportive due to a lack of access to complement inhibitor. These included blood transfusion, folate supplementation, cautious iron replacement and anticoagulation where indicated. One patient underwent successful matched sibling allogeneic stem cell transplant. This series highlights the presence of PNH in Kenya, diagnostic delay and the need for improved access to definitive testing and therapy in resource-limited environments. - Source: PubMed
Publication date: 2026/07/29
Ong'ondi MatildaLavender OtomGathinji MurayaBagha Zaheer