CD59 Antibody
- Known as:
- CD59 Antibody
- Catalog number:
- csb-ma0049471a0m
- 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
- Daratumumab, a human IgG1 monoclonal antibody targeting CD38, is widely used in multiple myeloma and AL amyloidosis. Despite its clinical success, many patients fail to achieve durable responses or relapse, underscoring the importance of understanding resistance mechanisms. Drawing on experience from other better-studied monoclonal antibodies, resistance to daratumumab can be categorized into four main mechanisms: (1) reduced CD38 expression on plasma cells; (2) increased expression of complement inhibitory proteins (CD55/CD59), impairing complement-mediated cytotoxicity; (3) reduced drug bioavailability due to urinary loss in non-selective nephrotic syndrome; and (4) the development of neutralizing anti-daratumumab antibodies. Anti-drug antibodies (ADAs) may represent a potential mechanism of treatment failure through effects on pharmacokinetics, efficacy, and safety, even in patients on daratumumab therapy. Seven different trials have tested anti-daratumumab antibodies. Among them, anti-daratumumab antibodies were identified in only 0-2.4% of patients, and only in a small portion of these has it been proven to be neutralizing. Overall, ADAs appear rare, but these findings are likely underestimated due to short follow-up and suboptimal timing of assessment. In conclusion, standardized ADA monitoring, particularly months after treatment interruption or in cases of inadequate response or infusion-related reactions, may improve patient management and therapeutic outcomes. - Source: PubMed
Publication date: 2026/07/03
Allinovi MarcoMalatesta LucaBiagioli TizianaAntonioli ElisabettaPerfetto Federico - Parkinson's disease (PD) is characterized by progressive degeneration of nigrostriatal dopamine neurons and synucleinopathy, which is the accumulation of aggregated α-synuclein (α-syn). Increasing evidence implicates α-syn-associated neuroinflammation as a contributor to PD pathogenesis, yet immune mechanisms linking synucleinopathy to neurodegeneration remain incompletely defined. Activation of the complement cascade occurs in PD and other synucleinopathies, but most studies report complement activation after overt neurodegeneration, making it difficult to conclude if complement is directly activated by pathological α-syn or secondarily following neurodegeneration. We used the rat α-syn preformed fibril (PFF) model, in vitro complement assays and postmortem human PD tissue to investigate whether pathological α-syn directly activates complement prior to overt neurodegeneration. The α-syn PFF model exhibits a protracted pathological time course and distinct temporal separation between peak α-syn aggregation and nigrostriatal degeneration. Thus, we quantified complement expression, activation, and regulation during the aggregation phase. Synucleinopathy caused complement activation prior to nigrostriatal degeneration, including upregulation of components of both the classical (C1qa, C1r, C4b) and alternative (Cfd, Cfb) pathways, the anaphylatoxin (C3aR, C5aR) and phagocytic (CR3) complement receptors, and activation of complement C3. During early synucleinopathy microglia upregulated C3, which significantly correlated with synucleinopathy burden across several brain regions, including the substantia nigra pars compacta (SNc) and cortex. Concurrently, complement regulators, including Cd55, Cd59, neuronal pentraxin-1 (Nptx1), and the neuronal pentraxin receptor were downregulated in the synucleinopathy-affected SNc. Importantly, increased levels of C1q and iC3b along with downregulation of CD55 and NPTX1 protein were also observed in human postmortem PD SNc tissue, supporting the translational relevance of our findings. Mechanistically, we demonstrate that aggregated, but not monomeric, α-syn directly binds C1q and activates the complement cascade in a C1q-dependent manner. These data provide the first in vivo evidence that synucleinopathy triggers complement activation and dysregulation prior to neurodegeneration. - Source: PubMed
Publication date: 2026/07/20
Khan HinaGifford MaryKordbacheh ArashBury AsherPanoushek SpencerCole-Strauss AllysonKemp Christopher JLuk Kelvin CSteece-Collier KathyKuhn Nathan CKanaan Nicholas MSortwell Caryl EPatterson Joseph RBenskey Matthew J - Oesophageal adenocarcinoma (EAC) is an aggressive malignancy in which the SWI/SNF catalytic subunits SMARCA2 and SMARCA4 are frequently lost, yet the biological and clinical impact of these deficiencies remains unclear. - Source: PubMed
Publication date: 2026/07/08
Grothey BastianKrämer MaxMontalbano MatteoLyu Su IrBruns Christiane JZander ThomasBüttner ReinhardQuaas Alexander - Prostate cancer (PCa) is a prevalent urological malignancy in men, with bone metastasis occurring in the majority of patients, often leading to poor clinical outcomes. Despite its clinical significance, reliable prognostic biomarkers for metastatic PCa remain limited. Immunogenic cell death (ICD), a regulated form of cell death, has emerged as a key modulator of the tumor immune microenvironment (TIME) and a potential determinant of the immunotherapy response. However, the functional role of ICD in PCa progression, particularly in bone metastasis, remains poorly understood. This study aimed to elucidate the prognostic implications of ICD in PCa and develop an ICD-correlated signature (ICDCS) model to improve risk stratification and therapeutic decision-making. - Source: PubMed
Publication date: 2026/07/07
Ma WeiguoMei WangliGuang LeiYang QinXu MingmingZhou Hang - Neuroinflammation can be triggered by traumatic brain injury (TBI) and exposure to toxicants such as chlorpyrifos (CPF), leading to chronic disabilities and substantial health care costs. CD59 and glial maturation factor-beta proteins are implicated in various brain regulatory mechanisms. Investigating their roles can provide valuable insights into their role in pathologies such as TBI. - Source: PubMed
Publication date: 2026/02/28
Castro-Vargas Rafael EnriqueHerrera-Sánchez María PaulaRondón-Barragán Iang