the shiga stx toxin is constituted by a subinudad a and five b the latter is the one that allows the binding to the gb3 and gb4 receptors that are glycosphingolipids, the A subunit is internalized and binds to the ribosimal 28s subunit and inhibits protein synthesis what causes death or apoptosis.
Very clear video! But I've a question about shiga-toxins. Many scientific articles have conflicting opinions about the link of the toxin to the Gb3 receptor. Some say what you say, others say that once released the toxin enters the bloodstream and from there it reaches receptors in the colon, kidneys and central nervous system. What do you think about that?
fimbria it is type 4 but the t3ss or pili type 3 is expressed thanks to the island of pathogenicity called LEE. which contains the information to express the proteins TIR (recipient of intimina trasmenbrane) t3ss is constituted by Esp A To this form a tube that allows the passage of Esp B and Esp D which open a pore in the menbrane of the enterocyte and allows the passage of Esp C or TIR. the external portion of TIR allows to bind to the intimin present in the membrane of the bacteria, the intramenbrane part of TIR causes the depolymerization of the actin which causes the pedestal structure to be formed and damage the integrity of the entocite.
the shiga stx toxin is constituted by a subinudad a and five b the latter is the one that allows the binding to the gb3 and gb4 receptors that are glycosphingolipids, the A subunit is internalized and binds to the ribosimal 28s subunit and inhibits protein synthesis what causes death or apoptosis.
straight to the point and very informative and helpful thanks man
Amazing illustration, Thank you!
Thank you very much!!
Very clear video! But I've a question about shiga-toxins. Many scientific articles have conflicting opinions about the link of the toxin to the Gb3 receptor. Some say what you say, others say that once released the toxin enters the bloodstream and from there it reaches receptors in the colon, kidneys and central nervous system. What do you think about that?
it helped me a lot, hugs from Brazil
You’re very welcome
Vera level explanation thank for the value able video
Good job!
Very clear and informative. Thank you!
Glad it was helpful!
Thank you very much
interesting video
Thank you
fimbria it is type 4 but the t3ss or pili type 3 is expressed thanks to the island of pathogenicity called LEE. which contains the information to express the proteins TIR (recipient of intimina trasmenbrane) t3ss is constituted by Esp A To this form a tube that allows the passage of Esp B and Esp D which open a pore in the menbrane of the enterocyte and allows the passage of Esp C or TIR. the external portion of TIR allows to bind to the intimin present in the membrane of the bacteria, the intramenbrane part of TIR causes the depolymerization of the actin which causes the pedestal structure to be formed and damage the integrity of the entocite.
thank you, EHEC mysteries solved!
Glad it helped, thank you
Ecoli: i dont feels so good =>
Thanks!!!!
⭐⭐⭐🌺
I don’t like those Shiga toxins
Tablat
Damn
Yeet
omg
elina
Thank you