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Health and Disease Semester 1 > Cell Signalling > Flashcards

Cell Signalling Flashcards

1
Q

What are the types of receptors?

A

Ion channels, G-protein coupled, receptor tyrosine kinases.

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2
Q

Give the domain topology of receptor tyrosine kinases?

A

Extracellular domain is based on an Ig like domain which is for binding to the ligand, they have a transmembrane domain and a carboxyl terminal domain which is in the cytosol for transmitting the signal by ligand induced conformational changes.

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3
Q

Upon binding of a ligand to a receptor tyrosine kinase what happens?

A

The cytoplasmic domain gains activity and transautophosphorylates a tyrosine residue using the phosphate from ATP to give tyrosine kinase intrinsic activity.

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4
Q

What do tyrosine kinase receptors recruit and why?

A

Lots of cytoplasmic proteins, to produce different signals.

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5
Q

What cytoplasmic protein bind to phosphorylated tyrosine?

A

SH2 and PTB

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6
Q

What cytoplasmic proteins bind to proline-rich sites?

A

SH3 and WW

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7
Q

What do PH cytoplasmic proteins bind to?

A

Different phosphoinositides.

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8
Q

What activity do cytoplasmic proteins recruited by the tyrosine kinase receptors have?

A

Variable, but some have no activity accept the role of a sub protein in order to recruit others.

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9
Q

How is Ras activated?

A

By the binding of SH2 to phosphorylated tyrosines

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10
Q

What is Ras?

A

A small, monomeric G-protein. It is also an oncogene.

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11
Q

What is Ras activation essential for?

A

Transmitting signals, as it activates mitogen activates protein kinase pathway (MAPK)

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12
Q

What do MAPK phosphorylate?

A

Serine or threonines

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13
Q

What is the MAPK pathway and what does it result in?

A 
Three steps: 
1. Ras-GTP form recruits Raf 
2. Causes phosphorylation of Mek
3. Causes phosphorylation of Er
this results in changes of gene expression and allows cells to respond to whatever growth factor is bound.
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14
Q

How do cells respond to the environment?

A

Via signal transduction cascades

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15
Q

Why is cancer became such a big problem?

A

We’re living longer so mutations accumulate over our lifetimes and way of living/environmental factors contribute.

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16
Q

Define a cancerous cell?

A

A cell that would reproduce defiance of the normal restraints of the cell division and growth.

17
Q

What do cancer cells do?

A

They outgrow and invade other organs preventing normal functions

18
Q

What are the causes of cancer?

A

Signal residing, 20-25% are caused by infectious agents (eg. Viruses) and some gave a genetic disposition.

19
Q

Give some examples of viruses that cause cancer?

A

Avian erythroblastosis virus, encodes a homolog of a growth factor that has been truncated through evolution and is turned on without a ligand binding event.
v-Erb2, upon infection it localises the plasma membrane and starts to signal and therefore activates.

20
Q

Give some examples of genetic dispositions causing cancers?

A

Mutant form of growth factors that lead to incorrect signalling but more common mutations in proteins, eg. Ras (30% of cancers) which is mutated and trapped in active GTP-bound form.

21
Q

What breakthroughs in cancer treatment have been developed?

A

Raf inhibitors BAY 43-9006 which acts in the MAPK pathway and inhibits it.
Herceptin is a Her2 receptor tyrosine kinase inhibitor which stops the signalling.

22
Q

What is a oncogene?

A

Any protein which can transform a cell.

23
Q

What is insulins role?

A

A pancreatic hormone that is essential for growth and development and vital for the control of glucose concentration, lipid metabolism in fat cells and protein metabolism.

24
Q

What is insulins receptor?

A

A receptor tyrosine kinase, transmembrane protein.

25
Q

What occurs when insulin binds to its receptor?

A

Insulin receptor substrates (IRS) undergo post translational modification and are phosphorylated to increase their protein-protein interaction. Pathways are initiated which reduce glucose transport and begin synthesis of glycogen to store the excess glucose.

26
Q

What are IRS proteins?

A

Insulin receptor substrate proteins, they mediated many of the metabolic function associated with insulin, particularly the PI3K pathways, and act as hubs for other proteins to bind.

27
Q

What is the PI3K pathway?

A

A lipid kinase phosphorylation pathway whic phosphorylates the 3’ hydroxyl of lipids and causes the formation of PIP3 lipid at plasma membrane and allows the requirement of many proteins with PH domains.

28
Q

What does the PI3K pathway lead to?

A

Enhanced glycolysis, protein synthesis and fatty acid biosynthesis.

29
Q

How is insulin signalling regulated?

A

Auto regulation: downstream enzymes inhibit upstream events using a negative feedback loop.
Desensitisation: unrelated recipe to pathway sends a signal to dampen down the signal that has been switched on, an unwanted effect.
Signals from free fatty acids and stress phosphorylate other serine and threonine residues on IRS proteins and blocks the signal.

30
Q

What are the symptoms of diabetes?

A

Frequent urination, increased thirst and hunger, dry mouth, nausea, fatigues, hyperinsulinemia, blurred vision, numbness and tingling in hands and feet and frequent infection of urinary tract and skin.

31
Q

What type of diabetes is insulin resistant?

A

Type 2

32
Q

What is type 2 diabetes usually associated with?

A

Obesity, CV disease, hypertension and chronic infection.

33
Q

What causes type 2 diabetes?

A

Genetic factors, polymorphisms in the multiple gene encoding proteins involved in insulin action, increased activity of lipid or tyrosine phosphatases that interfere with insulin signalling and serine/threonine phosphorylation of IRS proteins.

34
Q

What are high levels of free fatty acids in obese inhibitors of?

A

Insulin action, as they mediate the phosphorylation of IRS action on inhibitory sites.
Along with excess glucose they desensitise the PI3K pathway.

35
Q

What do adipocytes secreted factors do?

A

They antagonise the PI3K pathway to insulin stimulation.

36
Q

Why do pancreatic cells rely on the PI3K pathway?

A

As without it they are prone to apoptosis.

Health and Disease Semester 1 (14 decks)

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