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AB36467

APC Anti-CD59 抗体 [MEM-43]

APC Anti-CD59 antibody [MEM-43]

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(1 Publication)

Mouse Monoclonal CD59 antibody - conjugated to APC. Suitable for Flow Cyt and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Cell preparation containing CD59 protein.

別名を表示する

CD59, MIC11, MIN1, MIN2, MIN3, MSK21, CD59 glycoprotein, 1F5 antigen, 20 kDa homologous restriction factor, MAC-inhibitory protein, MEM43 antigen, Membrane attack complex inhibition factor, Membrane inhibitor of reactive lysis, Protectin, HRF-20, HRF20, MAC-IP, MACIF, MIRL

2 Images
Flow Cytometry - APC Anti-CD59 antibody [MEM-43] (AB36467)
  • Flow Cyt

Unknown

Flow Cytometry - APC Anti-CD59 antibody [MEM-43] (AB36467)

Flow Cytometry analysis of HL-60 (positive) and SP2 (negative) cells labeling CD59 with Anti-CD59 antibody [MEM-43] (Allophycocyanin) (ab36467).

Flow Cytometry - APC Anti-CD59 antibody [MEM-43] (AB36467)
  • Flow Cyt

Supplier Data

Flow Cytometry - APC Anti-CD59 antibody [MEM-43] (AB36467)

ab36467 (concentration in sample 1 µg/ml, red-filled histogram) binds specifically to CD59 expressed on surface of HL60 cells (upper panel), but not to surface of SP2 cells (lower panel).

Level of non-specific binding was assessed using Mouse IgG2a isotype control APC antibody (PPV-04) under same conditions (concentration in sample 1 µg/ml, black-dashed histogram).

関連する標識済み抗体及び組成の異なる製品 (1)

Key facts

宿主種

Mouse

クローン性

Monoclonal

クローン番号

MEM-43

アイソタイプ

IgG2a

軽鎖のタイプ

kappa

標識

APC

励起波長/蛍光波長

Ex: 650nm, Em: 660nm

キャリアフリー

No

交差種

Human

アプリケーション

Flow Cyt

applications

免疫原

Cell preparation containing CD59 protein. The exact immunogen used to generate this antibody is proprietary information.

P13987

エピトープ

Reacts with the well defined epitope (W40, R-53) on CD59 molecule

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "FlowCyt" : {"fullname" : "Flow Cytometry", "shortname":"Flow Cyt"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "FlowCyt-species-checked": "testedAndGuaranteed", "FlowCyt-species-dilution-info": "10 µL for 10^6 Cells", "FlowCyt-species-notes": "<p></p>" } } }

出荷温度及び保存条件

製品の状態
Liquid
精製度
IgG fraction
精製に関する特記事項
Purified antibody was conjugated with cross-linked APC under optimum conditions. The conjugate was purified by size-exclusion chromatography and adjusted for direct use.
バッファー組成
pH: 7.4 Preservative: 0.097% Sodium azide Constituents: 0.2% BSA
出荷温度
Blue Ice
短期保存温度
+4°C
長期保存温度
+4°C

補足情報

This supplementary information is collated from multiple sources and compiled automatically.

CD59 also known as protectin is a protein with a molecular mass of approximately 18-25 kDa. It is widely expressed on the surface of many human cells including red blood cells and various types of leukocytes. CD59 serves as an inhibitor of the complement membrane attack complex (MAC) preventing cell lysis caused by terminal complement proteins. Through this mechanism it regulates complement activation and maintains cell integrity by halting the formation of MAC.
Biological function summary

One important feature of CD59 is its role as a glycosylphosphatidylinositol (GPI)-anchored protein involved in safeguarding cells from complement-mediated damage. It does not exist within a larger complex but functions at the cell surface to inhibit the assembly of complement components C5b-9 which form the MAC. This ability to inhibit MAC is essential in maintaining self-tissue from unintended damage during immune responses.

Pathways

CD59 participates in the regulation of the complement cascade specifically within the terminal pathway. The complement system serves as a bridge between innate and adaptive immunity contributing to processes like opsonization and cell lysis. CD59's inhibitory action directly impacts pathways that utilize terminal components such as C5b. Effective CD59 function prevents excessive complement activation ensuring that an immune response does not damage host tissues. It links closely with other complement regulatory proteins like CD55 which also mitigate complement cascade activation.

Deficiencies or malfunctions in CD59 have notable implications. Paroxysmal nocturnal hemoglobinuria (PNH) is a disorder where lack of CD59 expression on blood cells leads to their increased destruction due to unregulated complement activity. Furthermore CD59's dysfunction or inadequacy also associates with atypical hemolytic uremic syndrome (aHUS) which involves mutant complement regulatory proteins causing overactivation of the complement system. These associations highlight the importance of CD59 in both maintaining cellular health and preventing pathophysiological conditions related to complement overactivity.

製品プロトコール

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ターゲットの情報

Potent inhibitor of the complement membrane attack complex (MAC) action, which protects human cells from damage during complement activation (PubMed : 11882685, PubMed : 1698710, PubMed : 2475111, PubMed : 2475570, PubMed : 2606909, PubMed : 9053451). Acts by binding to the beta-haipins of C8 (C8A and C8B) components of the assembling MAC, forming an intermolecular beta-sheet that prevents incorporation of the multiple copies of C9 required for complete formation of the osmolytic pore (PubMed : 11882685, PubMed : 1698710, PubMed : 36797260).. The soluble form from urine retains its specific complement binding activity, but exhibits greatly reduced ability to inhibit complement membrane attack complex (MAC) assembly on cell membranes.
See full target information CD59

文献 (1)

Recent publications for all applications. Explore the full list and refine your search

Scientific reports 2:345 PubMed22468229

2012

Functionally Distinct Subpopulations of CpG-Activated Memory B Cells.

Applications

Flow Cyt

Species

Human

Alicia D Henn,Michael Laski,Hongmei Yang,Stephen Welle,Xing Qiu,Hongyu Miao,Christopher T Barry,Hulin Wu,Martin S Zand
View all publications

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