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Cell Biology and disease > Strand 3 > Flashcards

Strand 3 Flashcards

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1
Q

What type of responses do cell surface receptors produce? Give examples.

A

Fast response eg ion channels, G protein coupled receptor and catalytic receptors.

Signalling molecule is hydrophilic and cannot cross the membrane.

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2
Q

What types of response do intracellular nuclear receptors produce? Give examples

A

Slow response eg regulate gene expression

Signalling molecule is hydrophobic

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3
Q

Which receptors do peptide and steroid hormones attach to ?

A

Peptide hormones eg insulin - cell surface receptors

Steroid hormone eg testosterone - intracellular (either cytoplasm or nucleus) receptor

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4
Q

The nicotinic receptor is an acetylcholine-gated sodium channel. Is this receptor inotropic or metabotropic and what does it control?

A

Inotropic - ligand gated ion channel. The receptor is both a receptor and ion channel at the same time.

When Ach binds to muscular nicotinic receptor, ion channel opens and Na+ enters cell, causing depolarisation and Ca2+ to be release from SR. This causes muscle contraction.

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5
Q

What are inotropic receptors?

A

Ligand gated ion channels. The receptor is both a receptor and ion channel at the same time.

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6
Q

What are metabotropic receptors?

A

G protein coupled receptors. When a ligand binds to the receptor, a separate ion channel is opened at some point ( they are not the same entity like inotropic)

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7
Q

What is the shortened name for gamma-amino buytyric acid receptor?

A

GABA A

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8
Q

What type of receptor is GABA A ?

A

Inotropic inhibitory receptor important in the brain.

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9
Q

What is Gaba A selective for and what activates Gaba A (inhibitory receptor) ?

A

Cl- ions. It is activated by benzodiazapines, alcohol and anesthetics.

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10
Q

Ach also binds to muscarinic receptors as well as nicotinic receptors. What type of receptor is the muscarinic Ach receptor?

A

Metabotropic. This receptor is sensitive to muscarine. There are 5 types (M1-M5)

M1,3,5 are stimulatory Gq
M2,4 are inhibitory Gi

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11
Q

What is the difference between GABA A and GABA B?

A

GABA B is metabotropic and activates a potassium channel, whereas GABA A is inotropic and activates Cl- channel.

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12
Q

Describe the G protein-coupled receptor pathway.

A
  1. When a ligand binds to the receptor, GDP (attached to the guanine nucleotide binding site on the alpha subunit) is exchanged with GTP, allowing the alpha subunit to dissociate from the Beta/gamma complex.
  2. The free alpha subunit activates adenylate cyclase, which produces cAMP.
  3. cAMP binds to regulatory subunits on PKA, causing the catalytic subunits to dissociate and phosphorylate other proteins.
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13
Q

What are 4 examples of physiological processes mediated by cAMP/PKA pathway?

A
  1. Kidney collecting duct - activated by vasopressin and stimulates water retention.
  2. vascular smooth muscle and cardiac muscle - activated by adrenaline, promotes relaxation of vascular smooth muscle and increases heart rate
  3. Colonic epithelium - activated by various factors and promotes fluid/ electrolyte secretion.
  4. Pancreas- activated by glucagon - promotes release of glucose.
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14
Q

What are ways of terminating the signal transduction?

A
  • removing signal
  • removing receptor
  • removing 2nd messenger
  • inactivation of activating signal proteins (GTP hydrolysis and dephosphorylation)
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15
Q

How to remove the 2nd messenger cAMP, and what will this do ?

A

Phosphodiesterase hydrolyses cAMP, so PKA tetramer is reassembled and signal transduction stops.

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16
Q

What inhibits Phosphodiesterases, and what activates it? (PDE) ?

A

Inhibited by caffeine

Activated by Ca2+/Cam (calmodium) complex.

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17
Q

How can the beta-adrenoreceptor which binds adrenaline be desensitised to stop the signal transduction?

A

PKA phosphorylates beta-ARK (adrenoreceptor kinase). Beta-ARK phosphorylates Beta-adrenoreceptor, reducing its affinity to adrenaline, therefore reducing the cellular response.

DAG can mediate desensitisation.

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18
Q

How can proteins be dephosphorylated to stop signal transduction?

A

protein phosphatases

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19
Q

In GPCR pathway, PKA phosphorylates CREB. What is CREB involved in?

A

Gene transcription

20
Q

The alpha subunit in GPCR can be stimulatory or inhibitory. How does cholera toxin affect GPCR?

A

Cholera toxin acts on alpha s and causes ADP-ribosylation. This prevents GTP hydrolysis which causes persistent activation of alpha subunit, and therefore consistent activation of PKA. This causes CFTR channel to open, so Cl- ions leave epithelial cell, and sodium and water follow to balance the charge - leading to diarrhoea.

21
Q

What does the pertussis toxin do to GPCR?

A

Acts on alpha inhibitory subunit and inhibits the inhibitory control of the alpha inhibitory subunit. This means that cAMP and PKA levels increase, as there is no control over it. In airways leads to symptoms of whooping cough.

22
Q

What two bacterial toxins act GPCR?

A
  1. Cholera toxin acts on alpha stimulatory subunit, prevents GTP hydrolysis, therefore constant activation of adenylate cyclase.
  2. Pertussis toxin acts on alpha inhibitory subunit, stopping the inhibitory effects, therefore cAMP and PKA levels increase.
23
Q

There are 3 different GPCR. Two (alpha stimulatory and alpha inhibitory) which involve cAMP and PKA. The 3rd type of GPCR is Gq, which involves phospholipase C (PLC). Describe this pathway.

A
  1. When a ligand binds to Gq protein, the alpha subunit dissociate and activates phospholipase C cleaves PIP2 into inositol 1,4,5 triphosphate (IP3) and diacylglyerol (DAG).
  2. IP3 is water soluble and travels through cytosol to ER, causing calcium to be released.
  3. DAG is hydrophobic and remains in the membrane, recruited protein kinase C (PKC).
24
Q

What are the two things Ca2+/CaM complex activates?

(calcium calmodium complex involved in Gq GPCR, PLC)

A
  1. Actiavtes PDE which degrades cAMP.
  2. Activates CaM kinases, which are involved in phosphorylation of serine and threonine residues, and also smooth muscle contraction.
25
Q

a1 adrenoreceptor is a Gq coupled protein receptor which mediates smooth muscle contraction. How does it do this?

A

PIP2 causes Ca2+ to be releases from ER. Ca2+ binds to calmodium making Ca2+/CaM complex, which activates CaMKs which cause smooth muscle contraction.

26
Q

Describe how a1 and B2 adrenoreceptors are involved in regulating blood pressure. Which type of receptors are a1 and B2?

A

a1 adrenoreceptor - Gq
B2 adrenoreceptor - Gs

a1 adrenoreceptors cause smooth muscle contraction (vasoconstriction) which increases blood pressure.

B2 adrenoreceptors cause vascular smooth muscle relaxation (vasodilation), therefore decreases blood pressure.

27
Q

What type of G protein receptor is the H1 histamine receptor?

A

Gq. Another receptor that causes smooth muscle contraction in the airways- important in asthma.

28
Q

a1/2 and B1/2/3 adrenoreceptors are G protein coupled receptors. Muscarinic receptors (M1-5) are also GPCR. Which ones are stimulatory and which ones are inhibitory, and which GPCR are they coupled to?

A

M1, M3, M5 - stimulatory. Activate PLC. Gq.

M2, M4 - inhibitory- inactivate AC which reduces cAMP. Gi.

29
Q

What does DAG directly activate?

A

PKC by phosphorylation.

30
Q

What are the 5 types of enzyme linked receptors?

A
  1. Receptor guanylyl cyclases
  2. Receptor serine/threonine kinase
  3. Receptor tyrosine kinase
  4. Tyrosine Kinase-associated receptors
  5. Receptor tyrosine phosphatase
31
Q

What is the normal amount of circulating glucose?

A

5mM

32
Q

What are the 3 types of cells in Islets of Langerhans in the pancreas?

A

a cells - produce glucagon
beta cells - produce insulin and amylin (most abundant cell)
gamma cells - produce somatostatin

33
Q

Insulin is synthesised as a polypeptide in the beta cells in the pancreas, and then is processed in the Golgi into pro-insulin, which is inactive. What enzyme activates this, and what happens to the insulin?

A

pro hormone convertase 1 and 2 removes the C chain from insulin. Insulin then becomes two polypeptide chains held together by disulphide bridges.

34
Q

Where is insulin stored?

A

Secretory granules in the beta cells, along with some pro-insulin and the C chain. The C chain can be used as a biological marker to indicate insulin secretion.

35
Q

What happens in beta cells when exposed to high circulating glucose (eg after meal) ?

A
  1. Glucose moves through GLUT transporters into beta cell and is phosphorylated to glucose 6 phosphate by glucokinase and then metabolised by glycolysis and mitochondrial oxidation to ATP.
  2. The beta cells have ATP-sensitive K+ channels which are open at normal levels of ATP. When glucose is high, ATP levels rise, so these channels close causing depolarisation.
  3. Depolarisation causes the voltage gated Ca2+ ion channels to open, causing Ca2+ to enter cell.
  4. All these steps cause beta cells to release insulin
36
Q

What is insulin released into from the pancreas?

A

Hepatic portal vein and therefore insulin goes to the liver first.

37
Q

The liver is normally impermeable to glucose. How does insulin change this?

A
  1. Increase in insulin released from pancreas binds to receptor tyrosine kinases on the surface of hepatocytes. Insulin induces activation of P13K, which activates protein kinase B (PKB).
  2. PKB causes GLUT4 transporters stored in vesicles to move to plasma membrane. Glucose can then move into cells through GLUT4 transporters.
38
Q

Once glucose has been taken up into the liver through GLUT4 transporters, it can be stored. If levels of glucose are high it will be stored, but if low it shouldn’t be stored. What enzymes are involved in this?

A

IF GLUCOSE HIGH -
Insulin activates PKB which phosphorylates GSK making it inactive. GSK normally will block glycogen synthase a , but if inactive, it cannot block glycogen synthase a so glycogen is made.

IF GLUCOSE LOW -
Glycogen synthase b will be phosphorylated by GSK meaning glycogen cannot be made.

39
Q

When glycogen storage is full in liver, excess glucose is converted to fat. How do you get rid of fat?

A

When glucose is not present, the body will use the fatty acids in metabolism. This will start to remove fat. However, if glucose is increased, the body will use glucose for metabolism and will not break down the fats.

40
Q

How does insulin promote the synthesis of new proteins?

A

Insulin activates P13K which targets ropamycin complex 1 (TORC1). TORC1 regulates protein synthesis in cells.

41
Q

When is glucagon released?

A
  1. when glucose is low
  2. during exercise. Exercise also promotes GLUT4 to move to surface of skeletal muscle so that more glucose can enter cell and can be metabolised to ATP.
42
Q

Glucagon receptor is a GPCR. What type of receptor is it and how does it promote release of glucose from liver?

A

Gs. cAMP pathway. Phosphorylase A produced which causes glycogenolysis. This pathway can also be activated by adrenaline acting on beta adrenoreceptors

43
Q

How does low glucose cause fat breakdown?

A

Low glucose causes glucagon release. Glucagon activates lipase which degrades fatty acids.

Remember insulin inactivates lipase so fats cannot be broken down.

44
Q

During starvation, glycogen stores are depleted, but glucose still needs to be made for the body somehow. How is glucose made during starvation?

A

Glucagon stimulates formation of glucose from lipids and amino acids. This process is gluconeogenesis

45
Q

Where is a glucagon receptor (Gs GPCR) not found?

A

skeletal muscle cells

Cell Biology and disease (4 decks)

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