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Cell Bio And Disease > Signalling In Disease > Flashcards

Signalling In Disease Flashcards

1
Q

Which 2 factors cause loss of control

A

Genetics eg mutations

Disease eg cholera or pertussis

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2
Q

Are all gpcr in all cells

A

No which causes either localised or systemic effects

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3
Q

How do gpcr change overtime

A

Levels of exp change during development

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4
Q

What are orphan receptors

A

Receptors that are close to structure as other gpcr but don’t have an identified ligand

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5
Q

Which 2 things cause hyperthyroidism

A

Overproduction of tsh/thyrotropin

Or failure of tsh gpcr to inactivate

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6
Q

What is the diabetes called which has lack of response /lack of ligand arginine vasopressin / ADH

A

Nephrogenic diabetes insipidus

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7
Q

What 3 things are in nephrogenic insipidus

A

Under production of ADH

Inability for receptor to recognise ligand

Inability for receptor to activate G protein to activate adenylyl cyclase

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8
Q

Where do ligands bind on gpcr

A

Exo loops or n terminal

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9
Q

What part of a gpcr binds with a G protein

A

Cytoloops and c terminus

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10
Q

What is bound to rhodopsin gpcr

A

11 CIS Retinal

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11
Q

What G protein associates which rhodopsin

A

Transducin

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12
Q

What happens to retinal and receptor when light hits

A

Converts 11 CIs to all trans retinal

And conformational change in receptor

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13
Q

What is the importance of activation of G protein transducin in rhodopsin

A

Activates pde converting cgmp to 5’gmp

This blocks the na cation channel and hyperpolarisation cell = activated neurone

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14
Q

What determines wavelength of light perceived by rhodopsin

A

Where retinal binds on the 7 tm domain on the lysine residue

The aa sequence surrounding it

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15
Q

How many aa determines diff between red and green wavelength perceived by rhodopsin

A

3 aa around the 7 tmd lysine where retinal binds

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16
Q

Why is red green colour blindness often in males

A

X linked and they need only 1

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17
Q

Why can recomb of red and green receptor genes occur

A

They are nearly homologous except 3 aa

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18
Q

Explain the 2 types of recomb occurring

A

Recomb where there’s unequal recomb and one x has more red copies and no green copies etc

Recombination within genes to form hybrids of red and green gene in one

19
Q

What G protein mutation causes night blindness

A

G a transducin (can’t activate pde)

20
Q

What g alpha subunit causes defects in blood clotting

A

G alpha 12

21
Q

What is caused by a mutation in a B3 subunit

A

Hypertension

22
Q

What mutation causes adrenal cortical tumours

A

Ai2

23
Q

What syndrome is caused by mutation in the g alpha s subunit (activates pka)

A

Mccune Albright syndrome

24
Q

What 2 diseases cause modification in g subunits

A

Cholera vibrio cholera - gas subunit

Pertussis bordatella whooping cough - gai subunit (inhibitory)

25
Q

What type of toxin is cholera

A

Hetero oligomeric - a and b exotoxin

26
Q

Which subunit of the cholera toxin enters cell

A

A subunit

27
Q

Which part of a subunit causes chemical mod of the gas subunit

A

CTa1 cholera toxin a1

28
Q

What does cta1 do to gas

A

Nad dependant adp ribosylation before the gtp site On a subunit

Causes constant activation of adenylyl cyclase

29
Q

How does cholera cause diarrhoea and dehydration

A

Camp increase causes Cl efflux out of cells

30
Q

What type of bacteria is cholera vibrio

A

Gram -ve rod

31
Q

What effect does increased camp have in cardiac

A

Increase in camp eg via SNS causes increase in contraction rate via increase in ca influx of ion channels etc

32
Q

How is camp important in kidney

A

V2 binding of ADH causes camp increase to increase aqueous channels in lumen for reabsorption

33
Q

What does camp do in bone when it’s increased by parathyroid binding

A

Increased reabsorption of ca in bone

34
Q

How does camp caused increase glucose

A

Lipolysis, phos of phosphorylase, phos of glycogen synthase

35
Q

How is phospholipase c terminated

A

Degradation into ip2 or phos into ip4

36
Q

How is type 2 diabetes different

A

Can produce insulin but they’re not responding to it

37
Q

What has been suggested to cause resistance

A

Increase in ffa/ fat diet/ increase in adipose cells

38
Q

Which populations have high type 2 occurrence

A

Pimas and aborigines

39
Q

Which hormones reduce appetite released by adipocytes

A

Leptin and adiponectin

40
Q

What tissue is the only one to increase overtime

A

Adipose

41
Q

What are adipokines for released for adipocytes

A

Lipid metabolism, appetite roles, glucose homeostasis, angiogenesis,immune system, ecm metabolism

42
Q

Is having no fat stores good

A

No also causes diabetes

43
Q

Why is mutations in signalling unlikely for type 2

A

Would be present at birth

44
Q

How is randles cycle / change in metabolic preferences a potential cause of diabetes

A

Competition of ffa and glucose to get b oxidated

If more fa then glucose can’t get oxidated and glycolytic enzymes get blocked

Cell Bio And Disease (18 decks)

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