cell communication (lec 1-3) Flashcards

1
Q

what are the three main things communication is needed for

A

development
homeostasis
breakdown

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2
Q

which type of signalling is like a whisper

A

contact dependant

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3
Q

which type of signalling requires an electrical connection

A

synaptic

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4
Q

which type of signalling uses gradients

A

paracrine

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5
Q

rank these in order of fastest to slowest
a)changing post translational modifications
b)changing structure of existing protein
c)changing protein via gene expression

A

b
a
c

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6
Q

why must target cells in endocrine signalling be specific

A

due to hormones being diluted in the bloodstream

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7
Q

which molecule is the precursor of most steroid hormones

A

cholesterol

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8
Q

what are the 2 classes of steroid hormones, give examples of each

A

corticosteroids(glucocorticoids and mineralocorticoids)

sex steroids(androgens, oestrogens, progesterones)

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9
Q

where are corticosteroids made

A

adrenal cortex

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10
Q

where are sex steroids made

A

gonads/placenta

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11
Q

what process occurs once the ligand has bound to a steroid hormone

A

translocation into the nucleus
act as transcription factors to regulate gene expression

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12
Q

what is the main type of receptor steroid hormones bind to

A

nuclear

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13
Q

what happens to primary response genes in secondary steroid signalling

A

they shut off

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14
Q

what is the process of cortisol being produced

A

CRH in hypothalamus
ACTH in pituitary
adrenal gland releases

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15
Q

what is cortisol

A

a glucocorticoid steroid hormone released in response to stress

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16
Q

what happens with primary adrenal sufficiency of cortisol

A

damage to the adrenal glands

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17
Q

what happens with secondary adrenal sufficiency of cortisol

A

lack of ACTH

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18
Q

how do you distinguish between primary and secondary adrenal sufficiency

A

give a shot of ACTH and if the person responds, they have secondary

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19
Q

what are the causes and symptoms of addisons disease

A

too little cortisol

depression, nausea, weight loss

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20
Q

what are the causes and symptoms of cushings disease

A

too much cortisol

weight gain, raised BP

21
Q

what is the process of insulin signalling

A

insulin binds to receptor(a RTK)

tyrosine phosphorylation of insulin receptor substates and proteins

binding of PI3K to p tyrosine sites, which synthesises PIP3

PIP3 recruits PDK, which directly phosphorylates AKT

AKT then Phosphorylates other substrates to ensure glycogen synthesis and glucose uptake

22
Q

how does metformin treat type 2 diabetes

A

activates AMPK

23
Q

which part of a TRK is hydrophilic

A

cyteine domain

24
Q

which part of a TRK interacts with downstream signalling machinery

A

tyrosine kinase domain

25
Q

what are the 2 different ways of transmitting info across a membrane

A

conformational change

dimerisation/multimerisation of transmembrane receptors

26
Q

which disease is associated with long term steroid abuse

27
Q

describe the phosphorylation of the insulin receptor

A

conformational change moves the 2 kinase domains closer together

kinase domains trans-phosphorylate

in addition, a closely associated docking protein insulin receptor substrate also becomes phosphorylated

28
Q

what is the main difference between intracellular receptors and cell surface receptors

A

intracellular are within cells
cell surface are on the cell surface

29
Q

which conserved elements does the hydrophilic domains of a TRK contain

30
Q

describe the transmembrane region of a RTK

A

20-25 aa of alpha helical structure

stabilised via interaction with fatty acid chains

31
Q

describe the RAS/RAF/MEK/ERK pathway

A

growth factors PDGF bind to RTKs on cell surface and cause phosphorylation(elbows)

the RTKs serve as docking sites for adapter proteins (grb2)

Grb2, via its SH2 and SH3 domains, recruits a type of GEF called SOS

SOS swaps GDP of GTP which activates Ras

Ras binds to inhibition domain of Raf which then activates itself

MEK is then activated which in turn activates ERK

pErk translocates into nucleus and triggers gene expression

32
Q

how is the Ras pathway regulated

A

by negative regulation

33
Q

how is Raf negatively regulated

A

by its own n terminal region
phosphorylation activates it

34
Q

how does Erk contribute to negative regulation

A

contributes to negative phosphorylation of Sos so prevent its binding to Grb2

35
Q

describe the location, activation and regulation of small GTPases

A

membrane tethered
activated by being bound to the GTP nucleotide
regulated by GEFs and GAPs

36
Q

what is the main function of the Ras family

A

relay signals from RTKs

37
Q

what is the main function of the Rho family

A

relay signals from surface receptors to cytoskeleton

38
Q

what do mutations in the Ras/Raf/MEK/ERK mainly cause

39
Q

How can you treat melanomas

A

use bRAF and MEK inhibitors

40
Q

what is the purpose of the JAK/STAT signalling pathway

A

immune system regulation

41
Q

What is a receptor associated tyrosine kinase

A

a receptor that itself doesnt have intrinsic phosphorylation properties

42
Q

describe the JAK/STAT singaling pathway

A

cytokines bind to RTKs/receptors associated with JAK kinases

dimerisation occurs which brings JAKs into proximity

STAT proteins doc to JAKs which leads to phosphorylation of specific tyrosine residues

43
Q

what is JAK and how many are present

A

a kinase

4

44
Q

what is STAT and how many are present

A

a signal transducer and activator of transcription

7

45
Q

What does the TPO pathway result in

A

platelet formation

46
Q

what does the EPO pathway result in

A

erythrocyte production(rbcs)

47
Q

what does mutant JAK2 cause

A

fibrosis in bone muscle

48
Q

how can fibrosis in bone marrow be treated

A

ruxolitinibs( a JAK2 inhibitor)

49
Q

where is Ras located

A

on the inner side of the plasma membrane