BIMM 110 Final Study Guide Questions
Exam 1 with complete solutions 2024/2025
Best way to study is to
Go to flashcard mode
Diabetes
Diabetes
In normal insulin signalling, which protein works just like Ras (from
Achondroplasia) and is activated by the nucleotide GTP?
a) IRS-1
b) PI3K
c) PIP3
d) Akt/PkB
e) Rab
e) Rab
Vessicular transport inside the cells is controlled by a large group of proteins
called Rab proteins that are controlled by the binding of nucleotides like GTP!
Review: What does Rab do?
Rab proteins control vesicle transport. They must be bound to GTP to be active
and they are controlled by GAP. GAP can be inhibited by AkT!
Once AkT is phosphorylated by PDK1 and PDK2, it is released into the cytoplasm
to do what?
a) To control vesicle transport
b) to inhibit Rab
c) To phosphorylate and inhibit the GAP that controls Rab
d) To phosphorylate and inhibit the GEF that controls Rab
c) to phosphorylate and inhibit the GAP that controls Rab.
,Review: What is the difference between GAP and GEF in normal insulin
signalling?
GAP works by hydrolyzing GTP into GDP+Pi which inhibits GTP-Rab binding and
thus prevents vesicle transport. So GAP prevents Rab from becoming active and
transporting vesicles to the membrane.
GEF does the opposite. GEP activates Rab by converting GDP+Pi into GTP.
True of False? AkT can function as an oncogene in addition to its function in
normal insulin signalling (phosphorylates and inhibits the GAP that controls Rab)
TRUEEEE
AkT and PI3K are both part of normal insulin signalling and cancer. AkT~
oncogene.
A lot of the time PI3K is overstimulated in cancer, especially breast cancer.
Ras~Achondroplasia
Rab~ Insulin signaling
Both are activated when bound to GTP.
Also, concerning FFA and how an excess of them in the bloodstream lead to
insulin resistance, after MD2 (FFA) binds to its receptor TLR4 on the target cell, it
activates a set of kinases including JNK from CTE!
What is special about the RTK of the insulin receptor on fat, muscle, and liver
cells that make it different from other RTKs?
The RTK insulin receptor is already dimerized even before the binding of insulin!
Upon the binding of insulin, the RTK activity is activated and the two kinases
phosphorylate all the tyrosine amino acids. These phosphorylations provide for a
docking site for the adaptor protein IRS-1.
Which is the correct sequence of events?
a) Insulin binds to the insulin receptor -> PI3K binds and is phosphorylated by the
kinase activity -> IRS-1 binds and adds a phosphate onto PIP2-> PIP3 which
brings akt/PkB close to the membrane where it is phosphorylated by PDK1&
PDK2-> Akt inhibits GAP and allows Rab+GTP complex to form -> Rab+GTP binds
to myosin motor proteins and transfer vesicles containing GLUT4 Transporters
along actin filament to the plasma membrane -> Glucose from bloodstream can
be transported into cytoplasm!
, b) Insulin binds to the insulin receptor -> IRS-1 binds, is phosphorylated by the
kinase activity of the insulin receptor, and adds a phosphate onto PI3K-> PI3K
adds a phosphate onto PIP2 -> PIP3 which brings akt/PkB close to the membrane
where it is phosphorylated by PDK1& PDK2-> Akt released into cytoplasm upon
phosphorylation and inhibits GAP and allows Rab+GTP complex to form -
>Rab+GTP binds to myosin motor proteins and transfer vesicles containing
GLUT4 Transporters along actin filament to the plasma membrane -> Glucose
from bloodstream can be transported into cytoplasm!
c) Insulin binds to the insulin receptor -> IRS-1 binds, is phosphorylated by the
kinase activity of the insulin receptor, and serves as a docking site for PI3K->
PI3K adds a phosphate onto PIP2 -> PIP3 (serves as a docking site for akt) which
brings akt/PkB close to the membrane where it is phosphorylated by PDK1&
PDK2-> Akt released into cytoplasm upon phosphorylation and inhibits GAP and
allows Rab+GTP complex to form ->Rab+GTP binds to myosin motor proteins and
transfer vesicles containing GLUT4 Transporters along actin filament to the
plasma membrane -> Glucose from bloodstream can be transported into
cytoplasm!
C. insulin -> insulin receptor -> IRS-1 -> PI3K -> PIP2 -> PIP3 -> akt/PkB ->
activated Rab -> GLUT4 on the plasma membrane.
What happens when insulin signalling is not functioning?
Glucose concentrations remain very high in the bloodstream.
Note: There could be increased activity of GAP (which inhibits Rab) OR
decreased activity of akt which would normally inhibit GAP.
What effect would a drug that permanently opens voltage gated Calcium channels
have on a diabetes patient?
Permanently opening VG Ca++ channels would trigger the insulin granules to
release intracellular insulin into the blood stream. This would lead to greater
insulin secretion that could counter insulin resistance in T2D
Between meals, pancreatic Beta cells produce and store insulin in __________.
intracellular vesicles called insulin granules.
What would happen if the ATP-sensitive K+ channels remain OPEN (in the
pancreatic beta cells)
There would be no intracellular depolarization which means VG Ca++ channels
would not open and trigger the release of insulin. So no insulin secretion!
Which test can you use to see the average level of blood sugar over the course of
3 months?
HbA1c glycated hemoglobin test.
Exam 1 with complete solutions 2024/2025
Best way to study is to
Go to flashcard mode
Diabetes
Diabetes
In normal insulin signalling, which protein works just like Ras (from
Achondroplasia) and is activated by the nucleotide GTP?
a) IRS-1
b) PI3K
c) PIP3
d) Akt/PkB
e) Rab
e) Rab
Vessicular transport inside the cells is controlled by a large group of proteins
called Rab proteins that are controlled by the binding of nucleotides like GTP!
Review: What does Rab do?
Rab proteins control vesicle transport. They must be bound to GTP to be active
and they are controlled by GAP. GAP can be inhibited by AkT!
Once AkT is phosphorylated by PDK1 and PDK2, it is released into the cytoplasm
to do what?
a) To control vesicle transport
b) to inhibit Rab
c) To phosphorylate and inhibit the GAP that controls Rab
d) To phosphorylate and inhibit the GEF that controls Rab
c) to phosphorylate and inhibit the GAP that controls Rab.
,Review: What is the difference between GAP and GEF in normal insulin
signalling?
GAP works by hydrolyzing GTP into GDP+Pi which inhibits GTP-Rab binding and
thus prevents vesicle transport. So GAP prevents Rab from becoming active and
transporting vesicles to the membrane.
GEF does the opposite. GEP activates Rab by converting GDP+Pi into GTP.
True of False? AkT can function as an oncogene in addition to its function in
normal insulin signalling (phosphorylates and inhibits the GAP that controls Rab)
TRUEEEE
AkT and PI3K are both part of normal insulin signalling and cancer. AkT~
oncogene.
A lot of the time PI3K is overstimulated in cancer, especially breast cancer.
Ras~Achondroplasia
Rab~ Insulin signaling
Both are activated when bound to GTP.
Also, concerning FFA and how an excess of them in the bloodstream lead to
insulin resistance, after MD2 (FFA) binds to its receptor TLR4 on the target cell, it
activates a set of kinases including JNK from CTE!
What is special about the RTK of the insulin receptor on fat, muscle, and liver
cells that make it different from other RTKs?
The RTK insulin receptor is already dimerized even before the binding of insulin!
Upon the binding of insulin, the RTK activity is activated and the two kinases
phosphorylate all the tyrosine amino acids. These phosphorylations provide for a
docking site for the adaptor protein IRS-1.
Which is the correct sequence of events?
a) Insulin binds to the insulin receptor -> PI3K binds and is phosphorylated by the
kinase activity -> IRS-1 binds and adds a phosphate onto PIP2-> PIP3 which
brings akt/PkB close to the membrane where it is phosphorylated by PDK1&
PDK2-> Akt inhibits GAP and allows Rab+GTP complex to form -> Rab+GTP binds
to myosin motor proteins and transfer vesicles containing GLUT4 Transporters
along actin filament to the plasma membrane -> Glucose from bloodstream can
be transported into cytoplasm!
, b) Insulin binds to the insulin receptor -> IRS-1 binds, is phosphorylated by the
kinase activity of the insulin receptor, and adds a phosphate onto PI3K-> PI3K
adds a phosphate onto PIP2 -> PIP3 which brings akt/PkB close to the membrane
where it is phosphorylated by PDK1& PDK2-> Akt released into cytoplasm upon
phosphorylation and inhibits GAP and allows Rab+GTP complex to form -
>Rab+GTP binds to myosin motor proteins and transfer vesicles containing
GLUT4 Transporters along actin filament to the plasma membrane -> Glucose
from bloodstream can be transported into cytoplasm!
c) Insulin binds to the insulin receptor -> IRS-1 binds, is phosphorylated by the
kinase activity of the insulin receptor, and serves as a docking site for PI3K->
PI3K adds a phosphate onto PIP2 -> PIP3 (serves as a docking site for akt) which
brings akt/PkB close to the membrane where it is phosphorylated by PDK1&
PDK2-> Akt released into cytoplasm upon phosphorylation and inhibits GAP and
allows Rab+GTP complex to form ->Rab+GTP binds to myosin motor proteins and
transfer vesicles containing GLUT4 Transporters along actin filament to the
plasma membrane -> Glucose from bloodstream can be transported into
cytoplasm!
C. insulin -> insulin receptor -> IRS-1 -> PI3K -> PIP2 -> PIP3 -> akt/PkB ->
activated Rab -> GLUT4 on the plasma membrane.
What happens when insulin signalling is not functioning?
Glucose concentrations remain very high in the bloodstream.
Note: There could be increased activity of GAP (which inhibits Rab) OR
decreased activity of akt which would normally inhibit GAP.
What effect would a drug that permanently opens voltage gated Calcium channels
have on a diabetes patient?
Permanently opening VG Ca++ channels would trigger the insulin granules to
release intracellular insulin into the blood stream. This would lead to greater
insulin secretion that could counter insulin resistance in T2D
Between meals, pancreatic Beta cells produce and store insulin in __________.
intracellular vesicles called insulin granules.
What would happen if the ATP-sensitive K+ channels remain OPEN (in the
pancreatic beta cells)
There would be no intracellular depolarization which means VG Ca++ channels
would not open and trigger the release of insulin. So no insulin secretion!
Which test can you use to see the average level of blood sugar over the course of
3 months?
HbA1c glycated hemoglobin test.
