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People and illness > week 4 > Flashcards

week 4 Flashcards

1
Q

Which amino acid does transcription always start with?

A

methionine

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2
Q

Which post translational modification targets protein for destruction?

A

ubiquitination

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3
Q

Describe lysosomal degradation

A

long half life
membrane proteins
extracellular proteins

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4
Q

describe proteosomal degradation

A

short half life
key metabolic enzymes
defective proteins

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5
Q

Describe primary proteins

A

sequence

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6
Q

describe secondary proteins

A

local folding

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7
Q

describe tertiary proteins

A

long-range folding

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8
Q

describe quarternary proteins

A

multimeric organisation

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9
Q

Describe supra molecular proteins

A

large scale assemblies

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10
Q

What is proteostasis?

A

protein homeostasis

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11
Q

What does proteostasis involve?

A 
synthesis 
degradation
localisation
trafficking
assembly 
processing
folding
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12
Q

Describe alpha helix formation

A

results from h bonds forming between carbonyl oxygen atom of each peptide bond with the amide H atom from an amino acid 4 positions toward the C terminus

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13
Q

Describe an alpha helix

A

periodic spiral
confers directionality
R groups face outwards, covering the helix

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14
Q

Describe beta pleated sheet

A

each strand is 5-8 amino acid residues
H bonding between strands of polypeptide forms the planar sheey
directionally parallel or anti-parallel
R groups project from both faces of the sheet

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15
Q

Describe how secondary proteins form

A

stabilised by interactions between R groupd
hydrophobic interactions between non-polar R groups
hydrogen bonds between polar R groups
disulphide bonds

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16
Q

Describe how proteins normally fold

A

assemble into 3D conformation
determined by its primary structure
hydrophobicity is an important determinant for final conformation

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17
Q

What are some of the problems with protein folding?

A

considerable variation in time taken for a protein to adapt to final conformation
cellular environment is highly crowded
increased tendency for proteins to aggregate

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18
Q

What is a molecular chaperone?

A

any protein that interacts with, stabilises, or helps another protein to acquire its functionally active conformation, without being present in its final structure

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19
Q

how do molecular chaperones work?

A

selectively bind to short stretches of hydrophobic amino acids

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20
Q

What are some proteome maintenance functions of molecular chaperones?

A

de novo folding
oligomeric assembly
protein trafficking
proteolytic degradation

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21
Q

What is the enzyme that detects problems with protein folding?

A

glucosyltransferase

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22
Q

What does glucosyltransferase detect?

A

hydrophobicity

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23
Q

What are the stages of the ubiquitin proteasome system?

A 
polyubiquitination
polyUb- protein recognised by CAP
polyUB removed; protein unfolded
protein threaded through proteasome
proteolysis
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24
Q

WHat is a proteinopathy?

A

accumulation of misfiled proteins resulting in aggregates, thereby gaining toxic activity or losing the normal function

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25
What are the genes involved in early onset familial AD?
amyloid precursor protein | presenilin 1, 2
26
What is the gene associated with sporadic AD?
apolipoproteinE e4 allele
27
What are the 2 abnormalities in protein in the brain of someone with AD?
amyloid plaques in extracellular space | neurofibrillary tangles in cytoplasm
28
What is the change in amyloid shape associated with AD?
change from alpha helix to beta sheet
29
What are the main components of neurofibrillary tangles?
paired helical filaments - tau
30
What are the physiological actions of Tau?
neurite outgrowth axonal transport microtubule dynamics
31
What are the pathological actions of tau?
neuronal fibrillary tangles microtubule dysfunction cell death
32
What are involved on the phosphorylation of tau?
cdk5 | GSK3beta
33
What is a proposed mechanism for tau aggregation?
``` detachment from microtubules misfiled tau pretangels b sheeted sheet containing structures neurofibrillary tangles ```
34
Describe dementia with lewy bodies
shares symptoms with AD and parkinson's disease presence of cortical lewy bodies alpha - synuclein aggregates
35
Describe a-synuclein in DLB
misfiling into beta pleated sheet structure that further aggregates into higher order insoluble structures; fibrils; the building blocks for lewy bodies
36
Describe transmissible spongiform encephalopathies
family of rare, progressive neurodegenerative disorders loss of motor control and behavioural changes can be inherited, sporadic or acquired long incubation periods characteristic changes associated with neuronal loss and failure to induce inflammatory resposnse
37
What is anterograde memory loss?
memory loss after disease sets in
38
What is retrograde amnesia?
old memories are forgotten
39
What is aphasia?
loss of language function
40
What is dysphagia?
impaired language function
41
What is agraphia?
loss of ability to write
42
What is alexia?
loss of ability to read
43
What is nominal dysphasia?
trouble naming objects
44
describe wernickes aphasia
fluent, fast, phonemic and semantic paraphasia, comprehension impaired, temporal lobe. receptive dysphasia
45
Describe brocas aphasia
non fluent, agramatic, phonemic paraphasias common, can't get words out, interior frontal lobe. comprehension is in tact
46
Where is important for visuospatial function?
right hemisphere
47
What is topographical disorientation?
dont know way around familiar environment
48
what is agnosia?
non recognition
49
what is prosopagnosia?
doesn't recognise face of people | may recognise smell, style of walking etc
50
What is included in cognition?
``` attention / orientation memory executive functioning language calculation praxis visuospatial ability ```
51
What are the different ways that attention can be classified?
arousal sustained attention divided attention selective attention
52
What tests can be used to assess attention?
``` orientation in time and place digit span reciting months of the year backwards serial 7s spell world backwards the STROOP test ```
53
What is the frontal lobe involved in?
``` goal setting and motivation judgement control of inhibtion flexibility and problem solving planning / sequencing organisation abstract reasoning social behaviour personality ```
54
Describe Wernicke's aphasia
fluent phonemic and semantic paraphasia comprehension impaired Wernicke's area (temporal lobe)
55
Describe broca's aphasia
non-fluent agramatic phonemic paraphasias common Broca's area (inferior frontal lobe)
56
What area of the brain is involved in calculation?
left hemisphere | angular gyrus in parietal lobe
57
WHat is acalculia?
inability to comprehend or write numbers properly
58
What is anarithmetria
difficulty with arithmetic
59
What types of dyspraxia are there?
errors in conception | errors in production
60
How can you test praxis?
imitation of gestures orobuccal movements use of imagined objects lower limb apraxia
61
What are common problems associated with visuospatial deficits?
``` topographical disorientation difficulties with dressing mis-reaching for objects visual neglect visual object agnosia prosopagnosia ```
62
WHat are the hallmark features of delirium?
``` impaired conciousness hyperactive or hypoactive subtype acute onset change in cognition visual hallucination sleep-wake cycle emotional changes in most cases, evidence of underlying direct cause ```
63
What are some of the precipitants of delirium?
``` infection stroke drugs MI fractures cancer electrolyte/fluid balance problems heart failure diabetes PVD alcohol withdrawal ```

People and illness (5 decks)

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