Anti-CD59 Antibody Picoband®(monoclonal, 3C10)

Overview

Anti-CD59 Antibody Picoband®(monoclonal, 3C10) is an antibody for CD59 detection raised in Mouse (Monoclonal, clone Clone: 3C10, Mouse IgG2b), with reported reactivity: Human. Commonly used in WB, IHC, IF, ICC, Flow Cytometry, ELISA workflows.

Key elements and design rationale

• Target: CD59 (CD59 glycoprotein); UniProt: P13987
• Antibody format: Mouse, Monoclonal, clone Clone: 3C10, Mouse IgG2b
• Molecular weight: 19 kDa
• Applications: WB, IHC, IF, ICC, Flow Cytometry, ELISA

Vendor description (summary): Boster Bio Anti-CD59 Antibody Picoband® (monoclonal, 3C10) catalog # M00914-2.

Biological background

Biological context: RNA-dependent helicase and ATPase required for nonsense-mediated decay (NMD) of mRNAs containing premature stop codons. Is recruited to mRNAs upon translation termination and undergoes a cycle of phosphorylation and dephosphorylation; its phosphorylation appears to be a key step in NMD. Recruited by release factors to stalled ribosomes together with the SMG1C protein kinase complex to form the transient SURF (SMG1-UPF1-eRF1-eRF3) complex. In EJC-dependent NMD, the SURF complex associates with the exon junction complex (EJC) (located 50-55 or more nucleotides downstream from the termination codon) through UPF2 and allows the formation of an UPF1-UPF2-UPF3 surveillance complex which is believed to activate NMD. Phosphorylated UPF1 is recognized by EST1B/SMG5, SMG6 and SMG7 which are thought to provide a link to the mRNA degradation machinery involving exonucleolytic and endonucleolytic pathways, and to serve as adapters to protein phosphatase 2A (PP2A), thereby triggering UPF1 dephosphorylation and allowing the recycling of NMD factors. UPF1 can also activate NMD without UPF2 or UPF3, and in the absence of the NMD-enhancing downstream EJC indicative for alternative NMD pathways. Plays a role in replication-dependent histone mRNA degradation at the end of phase S; the function is independent of UPF2. For the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed. The ATPase activity of UPF1 is required for disassembly of mRNPs undergoing NMD. Essential for embryonic viability.

Expression and localization notes: cellular localization: Nucleus. Cytoplasm. P-body., tissue context: Ubiquitous..

Common research applications

• Western blotting (WB): Compare CD59 levels across samples and conditions using appropriate loading and biological controls.
• Immunohistochemistry (IHC): Evaluate spatial distribution of CD59 in tissue sections, considering fixation and antigen retrieval effects.
• Immunofluorescence / ICC: Assess subcellular localization patterns and co-localization with compartment markers in cultured cells.
• Flow cytometry: Quantify CD59-positive populations in single-cell suspensions with appropriate gating and controls.
• ELISA: Use antibody-based detection formats to assess antigen presence or binding in plate-based assays.

Notes for experimental interpretation

• Account for isoforms, post-translational modifications, and sample-specific processing that can shift apparent molecular weight or epitope accessibility.
• Use positive/negative biological controls where possible (e.g., known-expressing cells/tissues, knockdown/knockout models) and include appropriate secondary-only/isotype controls for imaging workflows.

Additional product notes (from provided fields)

• Specificity: No cross reactivity with other proteins.
• Background: This gene encodes a cell surface glycoprotein that regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. And this protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It also plays a role in signal transduction pathways in the activation of T cells. Mutations in this gene cause CD59 deficiency, a disease resulting in hemolytic anemia and thrombosis, and which causes cerebral infarction. Multiple alternatively spliced transcript variants, which encode the same protein, have been identified for this gene.
• Cross reactivity: No cross-reactivity with other proteins.
• Cellular localization: Nucleus. Cytoplasm. P-body.
• Tissue details: Ubiquitous.
• Research category: Apoptosis,Cancer,Cardiovascular,G Protein Signaling,Heterotrimeric G Proteins,Neural Signal Transduction,Neurology Process,Neuroscience,Nucleotide Messenger,Second Messenger,Signal Transduction,Signaling Pathway,Small G Proteins

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.