CD59 ELISA kit
- Known as:
- CD59 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD59-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD59 ELISA kit
Related genes to: CD59 ELISA kit
- 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
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- The development of Alzheimer disease (AD) involves a cluster of pathogenic processes, including amyloid-beta (Aβ) deposition, tau-mediated neurodegeneration, chronic neuroinflammation, oxidative stress (OS), metabolic dysregulation, and disruption of circadian rhythms. Nuclear hormone receptor, Retinoic Acid-Related Orphan Receptor Alpha (RORα) was shown to regulate multiple neuroprotective pathways such as inflammatory signaling (NF-κB suppression), mitochondrial integrity and mitophagy, redox homeostasis [upregulation of glutathione peroxidase 1 (GPX1), and mitochondrial superoxide dismutase 2, (SOD2)], calcium-dependent synaptic architecture [inositol 1,4,5-trisphosphate receptor type 1 (ITPR1), Purkinje cell protein 4 (PCP4)], and circadian rhythm stability [period 2 (PER2), brain and muscle ARNT-like 1 (BMAL1)]. Multi-omics network analyses place RORα within regulatory networks that are co-associated with key AD-related genes and supports an associational, network-based relationship for . Preclinical gene-augmentation studies using adeno-associated viral vectors report that RORα overexpression reduces APP levels, remodels the complement regulator CD59 glycoprotein (CD59), inhibits OS, and enhances neuronal survival, although these effects were established largely in retinal and other non-AD systems. These findings support the potential of as a therapeutic target through genetic intervention, but direct demonstration of AD-modifying efficacy is still lacking. Investigational -focused gene therapy in retinal degenerative diseases provides proof-of-concept for, but does not yet establish, applicability within the central nervous system. Taken together, this evidence nominates as a candidate system-level regulator that may help restore disrupted homeostatic transcriptional networks in AD, a hypothesis that remains to be tested. We propose that RORα functions as a transcriptional hub coupling three homeostatic axes that fail in AD; the circadian, mitochondrial-metabolic, and immune-inflammatory axes, and that its regional expression changes in AD (hippocampal up-regulation vs. suprachiasmatic down-regulation) represent a compensatory response that ultimately fails. Cell-type-specific expression profiling is required to determine in which regions augmentation may be therapeutically appropriate. Restoring RORα is therefore could be network-stabilizing rather than single-pathway intervention. - Source: PubMed
Publication date: 2026/08/20
Chintalapally ShivakanthRajanala KalpanaUpadhyay Arun - The immunobiology of Guillain-Barré syndrome (GBS) has long been organized around a dichotomy: acute motor axonal neuropathy (AMAN) is an antibody-mediated nodal disorder, whereas acute inflammatory demyelinating polyneuropathy (AIDP) has been interpreted mainly through T-cell-mediated models of compact-myelin injury. Four successive findings challenge this separation. Intraneural injection of GBS sera produced demyelination without transfer of immune cells; pathological studies in AIDP localized complement activation to the Schwann-cell surface before macrophage-associated myelin stripping. Serum IgG from a substantial subset of patients with AIDP bound nodal or paranodal surface domains; and identification of gelsolin-3 defined an AIDP subset in which patient IgG, together with active complement, produced nodal disruption before internodal demyelination. Peripheral-myelin-reactive T cells further indicate that T-cell-mediated and antibody-mediated immunity may coexist. Within this evidence hierarchy, AMAN and a subset of AIDP have distinct initiating targets but converge on nodal dysfunction. CD55 and CD59 are membrane-bound complement regulators: CD55 limits complement amplification, whereas CD59 prevents assembly of the membrane attack complex. Both are detectable in compact myelin but not at human nodes of Ranvier, revealing a localized discontinuity in complement control. This local absence of complement regulators may influence whether antibody binding progresses to conduction failure, axonal degeneration, or internodal demyelination, but should be regarded as a permissive substrate for injury rather than as evidence of lesion localization. Observations in chronic inflammatory demyelinating polyneuropathy (CIDP) suggest that antibody-mediated functional injury may precede structural demyelination. This Review proposes complement-regulated nodal vulnerability to integrate evidence across AMAN and subsets of AIDP and CIDP while preserving differences in targets, tempo, and mechanistic strength. - Source: PubMed
Yuki Nobuhiro - 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