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Stonustoxin

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This lethal (towards mice) toxin induces hemolytic activities due to its ability to form pores in the cell membrane, elicits potent hypotension which is endothelium-dependent and appears to be mediated by the nitric oxide pathway and activation of potassium channels, displays edema-inducing activities, increases vascular permeability, induces endothelium-dependent vasorelaxation of isolated rat aorta, induces platelet aggregation, is myotoxic and interferes irreversibly with neuromuscular function.

Below are the list of possible Stonustoxin products. If you cannot find the target and/or product is not available in our catalog, please click here to contact us and request the product or submit your request for custom elisa kit production, custom recombinant protein production or custom antibody production. Custom ELISA Kits, Recombinant Proteins and Antibodies can be designed, manufactured and produced according to the researcher's specifications.
 

Stonustoxin subunit alpha

 Stonustoxin subunit alpha ELISA Kit
 Stonustoxin subunit alpha Recombinant
 Stonustoxin subunit alpha Antibody
Also known as Stonustoxin subunit alpha (SNTX subunit alpha).
This lethal (towards mice) toxin induces hemolytic activities due to its ability to form pores in the cell membrane, elicits potent hyp
>>>
otension which is endothelium-dependent and appears to be mediated by the nitric oxide pathway and activation of potassium channels, displays edema-inducing activities, increases vascular permeability, induces endothelium-dependent vasorelaxation of isolated rat aorta, induces platelet aggregation, is myotoxic and interferes irreversibly with neuromuscular function.
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Stonustoxin subunit beta

 Stonustoxin subunit beta ELISA Kit
 Stonustoxin subunit beta Recombinant
 Stonustoxin subunit beta Antibody
Also known as Stonustoxin subunit beta (SNTX subunit beta).
This lethal (towards mice) toxin induces hemolytic activities due to its ability to form pores in the cell membrane, elicits potent hypot
>>>
ension which is endothelium-dependent and appears to be mediated by the nitric oxide pathway and activation of potassium channels, displays edema-inducing activities, increases vascular permeability, induces endothelium-dependent vasorelaxation of isolated rat aorta, induces platelet aggregation, is myotoxic and interferes irreversibly with neuromuscular function.
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