CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

You are here

Products

back to search results

C5b9/TCC/MAC [aE11]

Product group: Primary
Monoclonal/ Polyclonal: Monoclonal
Clone: aE11
Host: Mouse
Isotype: IgG2a
Application: ELISA, Flow cytometry (FC), Immunocytochemistry (ICC),Immunofluorescence (IF), Immunohistochemistry (IHC)-F
Application notes: 10-50
Conjugation Type: Unconjugated
Lightchain type: Kappa
Reactivity: Human, Horse,Pig (Porcine), Monkey, Baboon
General notes: Localization: Secreted.
UNSPSC code: 12352203

The complement component proteins: C2, C3, C4 and C5 are potent anaphylatoxins that are released during complement activation. Binding of these proteins to their respective G protein-coupled receptors, C3aR, C1R and C5aR, induces proinflammatory events, such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. Activation of the complement system leads to the formation of C5b-9 terminal complex, and while C5b-9 can promote cell lysis, the sublytic assembly of C5b-9 on plasma membranes causes an opposite result and induces cell cycle activation and survival. C5b-9 can rescue oligodendrocytes from FAS-mediated apoptosis by regulating caspase-8 processing via PI 3-K signaling. C5b-9 may play a pro-inflammatory role in the acute phase of multiple sclerosis, but may also be neuroprotective during the chronic phase of the disease. (Shipping Cost: €200.00)

C5b9/TCC/MAC [aE11]

The complement component proteins: C2, C3, C4 and C5 are potent anaphylatoxins that are released during complement activation. Binding of these proteins to their respective G protein-coupled receptors, C3aR, C1R and C5aR, induces proinflammatory events, such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. Activation of the complement system leads to the formation of C5b-9 terminal complex, and while C5b-9 can promote cell lysis, the sublytic assembly of C5b-9 on plasma membranes causes an opposite result and induces cell cycle activation and survival. C5b-9 can rescue oligodendrocytes from FAS-mediated apoptosis by regulating caspase-8 processing via PI 3-K signaling. C5b-9 may play a pro-inflammatory role in the acute phase of multiple sclerosis, but may also be neuroprotective during the chronic phase of the disease.