CD59
- Known as:
- CD59
- Catalog number:
- 11-233-C025
- Product Quantity:
- 0.025 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
- Age-related macular degeneration (AMD) is among the leading causes of blindness worldwide. Early AMD is characterized by dysfunction in the choroid, including early dropout of endothelial cells and increased deposition of the complement cascade's membrane attack complex (MAC) in the choriocapillaris. In this study, we used a single-cell RNA sequencing-based approach with barcoded antibodies to measure abundance of the MAC and other surface proteins at single cell resolution on RPE/choroid samples from four aged human donor eyes. We included antibodies to detect the MAC, CD34, CD45, and complement regulators CD55 and CD59, in addition to control antibodies. Our analysis of these data revealed cell clusters with expected gene expression profiles and antibody-based detection of CD34 and CD45 congruent with transcriptome-based cell identity. We also detected surface complement regulators CD55 and CD59 across a wide variety of cell types. Across endothelial cells, surface CD55 and CD59 appeared more abundant on venous clusters, and abundance of each was correlated with expression of a third complement regulator, clusterin (CLU). The MAC was detected on a variety of cell types, but was most abundant on the surface of cells in the macrophage family, smooth muscle cells, and pericytes. We confirmed these findings by identifying MAC deposition on choriocapillaris pericytes using immunohistochemistry for MAC, endothelial, and pericyte markers. Ultimately, these data showcase a valuable new approach to analyze gene expression and surface complement in human donor eyes, and provide novel insight into patterns of MAC deposition and complement protection in the aging human choroid. - Source: PubMed
Publication date: 2026/09/10
Jensen Renato DMullin Nathaniel KMulfaul KellyMiller Jack E BNavratil EmmaVoigt Andrew PScheetz ToddWiley Luke AStone EdwinTucker BuddMullins Robert - Extracellular pH is a critical regulator of cell function in health and disease, yet tools for dynamic monitoring of pericellular pH at single-cell resolution remain limited. We report SurpHer, a genetically encoded, ratiometric extracellular pH biosensor identified through screening of a modular library of membrane-targeted designs. SurpHer combines the pH-sensitive fluorophore SEpHluorin with the reference fluorophore mKate2 and a CD59-derived GPI anchor, enabling robust plasma membrane localization, quantitative ratiometric imaging, and stable long-term expression. Unlike non-ratiometric membrane-targeted reporters, SurpHer corrects for variation in sensor abundance and imaging conditions, while avoiding the complexity and confounding sensitivities of FRET-based designs. SurpHer responds rapidly and reversibly across the physiologically relevant extracellular pH range of 6.0-7.8 and performs consistently in several human cell lines. Stable genomic integration enabled longitudinal imaging of extracellular pH gradients in a microfluidic tumor microenvironment model. SurpHer provides a versatile platform for investigating extracellular pH dynamics in complex biological systems. - Source: PubMed
Publication date: 2026/09/29
Holste Sofie CensSantos Leïla DosCharan Mahdi RezayatiNyhegn-Eriksen OlineCrouigneau RoxaneKragelund Birthe BMarie RodolpheSandelin AlbinAuxillos Jamie YamPedersen Stine Falsig - Alzheimer's disease (AD) and periodontitis (PD) are highly prevalent chronic disorders in ageing populations and share multiple pathological features, particularly persistent inflammatory and immune dysregulation. Despite increasing evidence supporting an association between the two diseases, the shared druggable molecular mechanisms underlying their comorbidity remain incompletely understood, and effective therapeutic strategies capable of simultaneously targeting shared disease-related processes are limited. This study aimed to identify shared druggable molecular candidates associated with AD and PD and to evaluate the potential biological effects of the natural products amentoflavone (AF) and taraxerone (TA) in AD-PD-related inflammatory cell models. An integrative strategy combining Mendelian randomisation (MR), transcriptomic profiling, machine learning, and structure-based virtual screening was used to identify and prioritise shared molecular candidates associated with AD and PD. Molecular docking and molecular dynamics (MD) simulations were performed to evaluate the predicted binding modes and interaction stability of AF and TA with selected core proteins. In vitro experiments were conducted using LPS-induced mouse BV2 microglia and mouse primary gingival fibroblasts (MGFs) to assess the effects of AF and TA, alone and in combination, on core-gene expression, inflammatory mediator secretion, oxidative stress, apoptosis, and iNOS/CD206-defined microglial activation states. MR, transcriptomic, and machine-learning analyses prioritised six shared key genes, including FCGRT, LTBP1, CD59, SPRED1, SURF2, and ZDHHC2, with FCGRT, SPRED1, and SURF2 selected for subsequent structural and cellular investigations. Molecular docking and MD simulations suggested stable predicted interactions of AF and TA with these three proteins. AF formed persistent hydrogen-bond networks, particularly in the SPRED1 and SURF2 complexes, whereas TA interactions were predominantly hydrophobic. MM-PBSA analysis yielded favourable binding free energies ranging from - 62.4 to - 99.7 kJ/mol. AF at 10 µM and TA at 20 µM were selected as non-cytotoxic working concentrations for subsequent cellular experiments. Both compounds partially restored LPS-associated alterations in FCGRT, SPRED1, and SURF2 expression, reduced TNF-α, IL-1β, and IL-6 secretion, increased IL-10 production, attenuated oxidative stress by reducing ROS, MDA, and NO levels while increasing SOD activity, decreased apoptosis, and shifted the iNOS/CD206-defined microglial activation profile away from an LPS-induced pro-inflammatory state toward an anti-inflammatory or repair-associated response. AF + TA co-treatment produced greater combined effects than either single treatment in several assays; however, quantitative combination analyses are required to determine whether these effects represent pharmacological synergy or additive interactions. This study identified FCGRT, SPRED1, and SURF2 as prioritised shared molecular candidates associated with AD and PD and provided computational and cellular evidence supporting further investigation of AF and TA as potential natural-product-based therapeutic candidates. AF and TA showed stable predicted interactions with the selected proteins and modulated gene-expression, inflammatory, oxidative-stress, apoptotic, and microglial-activation-related phenotypes in LPS-induced cellular models. These findings provide additional insight into the shared molecular landscape of AD and PD and support further experimental evaluation of AF and TA, including direct target-engagement studies, quantitative combination analyses, and in vivo validation. - Source: PubMed
Publication date: 2026/09/29
Wu YekeLi ShuangZhang XimeiXu QianrongChen BingjunYang WenbinLiu MinLi JiaweiHe XiangLi JuanWu Wenbin - Mpp46Aa1 (formerly PS2Aa1) is a β-pore-forming protein produced by Bacillus thuringiensis that exhibits selective cytotoxicity against cancer cells. Protein engineering has generated variants with improved antitumor activity, including the N65 variant, which contains three amino acid substitutions. - Source: PubMed
Publication date: 2026/09/15
Bravo-Granados Natalia ARueda-Forero Nohora JulianaVisser LydiaSuárez-Barrera Miguel O - Corneal hyperglycemia is associated with epithelial dysfunction characterized by impaired inflammation, oxidative stress, neuropathy and innate immune mechanisms, as observed in diabetic corneal keratopathy. Therefore, the aim of the study was to investigate at cellular level the effects of moderate to severe acute and chronic challenges of glucose on human primary cultures of corneal epithelial cells (CECs). Human CECs (Innoprot, Spain) were exposed to single or repeated 15 mM or 30 mM High Glucose (HG)-supplemented media (CEC Medium containing plain 5 mM glucose), every 2 days from first stimulations and harvested at day 1 (single/acute challenge) or at days 3 and 5 (repeated/chronic challenge). Mannitol was used as osmotic control and cell sustainability were monitored by trypan blue exclusion test and MTT. Conditioned media were subjected to protein analysis while monolayers were processed for relative real-time RT-PCR. Few selected mediators belonging to the inflammatory, complement, innate receptor, oxidative, DNA enzymes and neurotrophic pathways were tested, and protein levels were assayed on selected mediators (IL-6, IL-8, CFH and C5b-9; ELISA). HG exposure induced a time- and concentration-dependent decrease in CEC metabolic activity, without a comparable reduction in cell number. Acute HG exposure promoted an inflammatory response characterized by increased , , and transcripts, together with an early modulation of complement components and increased expression of and (regulators). Chronic HG exposure induced a marked shift toward complement activation, with increased , , , and transcripts and reduced and expression, with a progressive accumulation of CFH and C5b-9 proteins in a positive relationship. Chronic HG also increased IL-6 and IL-8 protein release and induced a coordinated upregulation of , and , particularly at 30 mM HG. Antioxidant, DNA enzymes and neurotrophic pathways were differentially modulated over time, with an early response followed by chronic upregulation and reduction, progressive / expression, and a biphasic / transcriptional profile. Overall, these findings support a proposed biphasic model of the CEC response to hyperglycemia, characterized by an initial adaptive molecular response followed by progressive dysregulation under prolonged exposure. This early molecular profile might represent an adaptive response to acute metabolic stress, although further studies are required to confirm this functional protective significance. - Source: PubMed
Publication date: 2026/09/21
Dinice LuciaBalzamino Bijorn OmarEsposito GrazianaSquitti RosannaDi Zazzo AntonioMicera Alessandra