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Cell Proliferation and Underlying diseases > Protein phosphorylation and other post translational modifications > Flashcards

Protein phosphorylation and other post translational modifications Flashcards

(49 cards)

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1
Q

How is the dynamic-rapid response achieved?

A

Post translational modifications and not gene transcription regulation (takes too long)

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2
Q

What are post translational modifications?

A

Covalent modifications after translation

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3
Q

What is the eraser of ubiquitination?

A

Deubiquitinases (DUBs)

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4
Q

What are the 3 ubiquitin enzymes?

A

E1 - ubiquitin activating enzyme
E2 - ubiquitin conjugating enzyme
E3 - ubiquitin ligase

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5
Q

What are the 3 types of ubiquitination?

A
  • monoubiquitylation
  • multi-monoubiquitylation
  • polyubiquitylation
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6
Q

What are the four types of conformational change?

A

Local disruption
Local ordering
Long-range disruption
Long-range ordering

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7
Q

What are the effects of PTMs?

A

Conformational changes

Protein:protein interactions

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8
Q

Examples of protein:protein interactions

A

14-3-3 protein
bromodomains
SH2
PHD domains

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9
Q

What is the writer for acetylation?

A

Acetyltransferase

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10
Q

What is the eraser for acetylation?

A

deacetylase

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11
Q

What is the writer for methylation?

A

methyl-transferase

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12
Q

What is the eraser for methylation?

A

amine oxidase
demethylase
deiminase

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13
Q

What is the writer for proline hydoxylation?

A

prolyl hydroxylase

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14
Q

What are the roles of PTMs?

A 
Activity 
Localisation 
Stability 
DNA/ RNA binding 
Complex formation 
Selectivity
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15
Q

Example of PTM selectivity

A

PTM control selective activation of particular p53 target genes

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16
Q

Types of PTM crosswalk

A

Positive crosswalk

Negative crosswalk

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17
Q

What is positive crosswalk?

A

one PTM is a signal for the addition or removal of a second PTM

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18
Q

What is negative crosswalk?

A

Mutually exclusive - Direct competition for modifying a single residue
Antagonistic - indirectly by changing the recognition site for another PTM

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19
Q

How are PTMs measured?

A

Mass spec

Antibodies

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20
Q

What is mass spec?

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A

An analytical tool which ionises chemical species and sorts the ions based on their mass-to-charge ratio.
Used to elucidate the chemical structures of molecules.

21
Q

How does mass spec work globally and on individual proteins?

Study These Flashcards
A

Sample undergoes gas/ liquid chromatography
Undergo ionisation interface
Undergo mass spec

22
Q

How does mass spec work on only individual proteins?

Study These Flashcards
A

Sample undergoes enzimatic digestion to form peptides
Undergoes gas/ liquid chromatography
Undergo ionisation interface
Undergo mass spec

23
Q

Advantages of mass spec

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A
  • unbiased/ untargetted information
  • can differentiate very similar proteins/ isoforms
  • can generate a huge amount of information
  • quantitative
24
Q

Disadvantages of mass spec

Study These Flashcards
A
  • expensive and time consuming
  • hard to pinpoint the position of the phosphorylation site
  • very abundant proteins will mask low abundance proteins
  • need expertise e.g. equipment
25
What do antibodies recognise?
the modified group and part of the peptide surrounding it
26
What modifications can antibodies recognise?
Methylation Acetylation Phosphorylation
27
What modifications can antibodies not be used for?
Ubiquitylation | SUMOylation
28
Advantages of using antibodies
- cheap if they are available - specific - very sensitive - can identify subtle differences - give quantitative information
29
Disadvantages of using antibodies
- need to already know where it is modified and what type of modification - not antibodies available for each modified protein - producing new antibodies is expensive, time consuming and not always successful
30
What is the basic structure of a protein kinase?
Conserved core 2 lobes The active site (where the ATP binds) in the cleft between the two lobes
31
What happens in the inactive form of a kinase?
C-helix out R-spine disassembled Activation loop disordered
32
What happens in the active from of a kinase?
C-helix in R-spine assembled Activation loop ordered
33
What determines kinase specificity?
The depth of the catalytic cleft Peptide specificity Distal docking sites Targetting subunits
34
How is peptide specificity determined?
depends on the kinase P+1 loop sequence
35
What is distal docking sites mediated through?
binding domains outside the kinase active site and the substrate phosphorylation site
36
explain targetting subunits
binding partners that contain docking domains that help to target the kinase to specific substrates
37
What happens to tyrosine kinases in tumour cells?
Deregulated: - hyperactivating mutations - amplifications/ overexpression - loss of negative regulation
38
what are the two types of protein kinase inhibitors?
- Non-covalent inhibitors | - Covalent inhibitors
39
What are the types of non-covalent inhibitors?
Type I - ATP-competitive = bind to the active conformation Type II - non-ATP-competitive - bind to inactive conformation Type III and IV - non-ATP- competitive - bind outside the ATP binding site (allosteric inhibition)
40
Describe covalent inhibitors
Bind to the ATP-binding site Not ATP competitive Low selectivity
41
Describe the use of chemical probes
- ask a specific biological question - need biological validation - need specificity - need to have a define mechanism of action - bioavailability not needed
42
Describe the use of drugs
- need to be clinically safe and effective - need clinical validation - does not need to be specific - do not need a define mechanism of action - need human bioavailability and good pharmacokinetics
43
What are the two types of resistance?
Primary resistance | Acquired resistance
44
Explain primary resistance
de novo lack of treatment response
45
What are the types of acquired resistance?
- Target gene amplification - Target secondary mutations - Chromosomal alterations - Bypass of drug alteration
46
Explain target gene amplification
Where the target is upregulated e.g. more kinase = drug less effective
47
Explain target secondary mutations
mutations which result in reduced effectiveness to the drug
48
Explain chromosomal alterations
Alternative splicing to hyperactive chimeric or truncated kinase
49
Explain bypass of drug inhibition
Amplification of downstream signalling mediator

Cell Proliferation and Underlying diseases (12 decks)

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