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T5319

Sigma-Aldrich

Tetanolysin from Clostridium tetani

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About This Item

CAS Number:
MDL number:
UNSPSC Code:
12352200

biological source

Clostridium tetani E88

mol wt

55 kDa

application(s)

cell analysis

storage temp.

2-8°C

Gene Information

Clostridium tetani E88 ... CTC01888(1060232)

General description

Hemolytic activity of tetanolysin is determined using 2.5% rabbit red blood cells at 37 °C for 40 min.

Application

Tetanolysin has been used to analyze the formation of lytic pores in red blood cells (RBCs)1. It has also been used to permeabilize infected RBCs2.

Biochem/physiol Actions

Cholesterol-binding toxin used to permeabilize cellular membranes to enhance the entry of macromolecules into the interior of the cell. Pores induced reported to be in the range of 20-50 nm.

Preparation Note

Prepared by a modification of the method of Haque, et al.

Reconstitution

When reconstituted with 100 μl of sterile water the concentration is 1 μg/μl in 40 mM sodium phosphate buffer, pH 7.2, containing 200 mM NaCl.

Analysis Note

Single band by SDS-PAGE.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Hayley E Bullen et al.
The Journal of biological chemistry, 287(11), 7871-7884 (2012-01-19)
To survive within its host erythrocyte, Plasmodium falciparum must export hundreds of proteins across both its parasite plasma membrane and surrounding parasitophorous vacuole membrane, most of which are likely to use a protein complex known as PTEX (Plasmodium translocon of
Jason W Rosch et al.
The Journal of clinical investigation, 120(2), 627-635 (2010-01-23)
Sickle cell disease (SCD) is characterized by intravascular hemolysis and inflammation coupled to a 400-fold greater incidence of invasive pneumococcal infection resulting in fulminant, lethal pneumococcal sepsis. Mechanistically, invasive infection is facilitated by a proinflammatory state that enhances receptor-mediated endocytosis

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