BIO-0046 Lecture Notes - Lecture 7: Immunosuppressive Drug, Thapsigargin, Calcineurin
Document Summary
Thapsigargin rescues defects if they occur before the er. However ca2+ channel on the plasma membrane is broken, so. Er release -> ca2+ channels on plasma membrane open. Two patients were helpful because they were broken so we could see the normal pathway. Chemical structure -> how to go after it to inhibit it. Et-1 is a ligand for a gpcr expressed on the cells used in the below experiment. Six samples of cells were treated with ligand for varying fme periods (0-30") Gpcr is getting desensitized by arrestin, so that"s why we start to fade at the end- we"re losing activity from gpcr. Gpcr activated a kinase, which then went off and phsophorylated the tail of her1, allowing you to recruit sh2 domains, etc. Make decision here about where to send receptor. Therefore, this is the spot where receptor and ligand separate! Ligand degraded, receptor recycled back to surface and used again.
