cellular signaling : response to insulin

Question 1

insulin

Answer 1

receptor is an RTK (receptor tyrosine kinase) but different from other RTK’s as permanently dimerized.
complex signaling pathway…

Question 2

Insulin receptor

Answer 2

permanently dimerized.

IRS-1 and IRS-2 (insulin receptor substrate) has tyr that gets +Pi, do has Pi3K protein that gets activated, which eventually activates PKB (same thing as Akt). PKB is able to be inhibited/activated. PKB inhibits GSK3

if GSK3 is active (GSK3 not +Pi), will cause GS to go from active to inactive forms. (Insulin activates GS by inhibiting GSK3 which would have +Pi GS and inhibit it)

Question 3

Vescicle

Answer 3

cellular pinchoff, contains membrane with glucose transporters. When high BS, want gluc transports to fuse with the membrane of vescicle to bring glucose in. WHen low GS levels, want these to be pulled away, especially in muscle because they are passive transporters and dont want them going in opposite direction..

GLUT 4, muscle transporter, do not want too many transporters on the outside of the cell… high BS want the vescicle to stick to them and bring in Glucose.

Question 4

cascade

Answer 4

Insulin activates IRS2, Pi3K is activates, PKB is activated which inhibits GSK3 … so activation of glycogen synthesis (because PKB inhibits GSK3)?

Question 5

PKB also inhibits…

Answer 5

the transcription of PEPCK/G6Pase catalytic subunit, because dont want PEPCK and G6Pase to be active when there is High BS