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- CAN
Ships within 48 hours · Estimated delivery Jul 7 - Jul 12
For Your Every Summer RSVP, with Code: SUMMER15
Description
FITC Mouse Anti-Human CD55 Antibody (S-3120)Product Specification Host Mouse Antigen DAF CD55 Synonyms Complement decay accelerating factor; CR; DAF Location Cell membrane Accession P08174 Clone Number S 3120 Antibody Type Mouse mAb Isotype IgG2a,k Application FCM Reactivity Hu Positive Sample human peripheral blood Leukocytes Purification Protein A Concentration 0. 2 mg ml Conjugation FITC Physical Appearance Liquid Storage Buffer PBS, 1% BSA, 0. 3% Proclin 300 Stability & Storage 12 months
Product Specification
| Host | Mouse |
| Antigen | DAF/CD55 |
| Synonyms | Complement decay-accelerating factor; CR; DAF |
| Location | Cell membrane |
| Accession | P08174 |
| Clone Number | S-3120 |
| Antibody Type | Mouse mAb |
| Isotype | IgG2a,k |
| Application | FCM |
| Reactivity | Hu |
| Positive Sample | human peripheral blood Leukocytes |
| Purification | Protein A |
| Concentration | 0.2 mg/ml |
| Conjugation | FITC |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 1% BSA, 0.3% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
| application | dilution | species |
| FCM | 5μl per million cells in 100μl volume | Hu |
Background
Decay-accelerating factor (DAF, also known as CD55) is a complement regulatory protein that plays a crucial role in protecting cells from complement-mediated attack. It is a membrane lipid microdomain-associated, GPI-anchored protein that accelerates the decay of C3 and C5 convertases, which are essential for the downstream formation of the membrane attack complex (MAC) in the complement cascade. This action helps prevent excessive complement activation and subsequent cell damage. CD55 is involved in various physiological and pathological processes, including immune regulation, cancer progression, and tissue protection. In cancer, CD55 can promote malignant transformation, cell survival, angiogenesis, and inhibit apoptosis through intracellular signaling pathways such as JNK, JAK/STAT, MAPK/NF-κB, and LCK. Additionally, it is enriched in the cancer stem cell niche and can be induced by chemotherapeutics and hypoxic environments.
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Exchange/Return Notes
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