The sequential model definitely requires conformational changes. The shape change of one subunit due to substrate binding directly impacts and drives the neighboring subunit to change to the relaxed form and promotes ligand binding there as well. The concerted model is less dependent on the conformational change itself since it’s driven by an equilibrium of states.
God bless you no one needs lehninger when you are here
God bless you!! You're the best!!
Thank you, great explanation ! 💕
Very helpful :D Thanks!
Fr the best explanation ever ❤
What a G. Very fluent explanation. Puts my Biochem professor to shame!
Thanks so much, Any! Appreciate the kind words and support!
Thanks you, you helped me in my assignment
Thank you so much. Well explained❤
Do you happen to have the link to the online tutorial as mentioned in the video?
Well explained 👍🏻👍🏻👍🏻👍🏻
Why can the sequential model only account for the negative homotropic allosteric effectors?
wouldnt all enzymes be considered allosteric because they change shape when they bind to a substrate?
I don’t understand how (or if) these models depends on the actual modification induced by the binding with the ligand
The sequential model definitely requires conformational changes. The shape change of one subunit due to substrate binding directly impacts and drives the neighboring subunit to change to the relaxed form and promotes ligand binding there as well. The concerted model is less dependent on the conformational change itself since it’s driven by an equilibrium of states.
@@thomasmennella5501 well said here