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More mol and cell > cell communication (lec 1-3) > Flashcards

cell communication (lec 1-3) Flashcards

(49 cards)

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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

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A

too much cortisol

weight gain, raised BP

21
Q

what is the process of insulin signalling

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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

Study These Flashcards
A

activates AMPK

23
Q

which part of a TRK is hydrophilic

Study These Flashcards
A

cyteine domain

24
Q

which part of a TRK interacts with downstream signalling machinery

Study These Flashcards
A

tyrosine kinase domain

25
what are the 2 different ways of transmitting info across a membrane
conformational change dimerisation/multimerisation of transmembrane receptors
26
which disease is associated with long term steroid abuse
cushings
27
describe the phosphorylation of the insulin receptor
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
what is the main difference between intracellular receptors and cell surface receptors
intracellular are within cells cell surface are on the cell surface
29
which conserved elements does the hydrophilic domains of a TRK contain
Ig s EGFs
30
describe the transmembrane region of a RTK
20-25 aa of alpha helical structure stabilised via interaction with fatty acid chains
31
describe the RAS/RAF/MEK/ERK pathway
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
how is the Ras pathway regulated
by negative regulation
33
how is Raf negatively regulated
by its own n terminal region phosphorylation activates it
34
how does Erk contribute to negative regulation
contributes to negative phosphorylation of Sos so prevent its binding to Grb2
35
describe the location, activation and regulation of small GTPases
membrane tethered activated by being bound to the GTP nucleotide regulated by GEFs and GAPs
36
what is the main function of the Ras family
relay signals from RTKs
37
what is the main function of the Rho family
relay signals from surface receptors to cytoskeleton
38
what do mutations in the Ras/Raf/MEK/ERK mainly cause
melanomas
39
How can you treat melanomas
use bRAF and MEK inhibitors
40
what is the purpose of the JAK/STAT signalling pathway
immune system regulation
41
What is a receptor associated tyrosine kinase
a receptor that itself doesnt have intrinsic phosphorylation properties
42
describe the JAK/STAT singaling pathway
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
what is JAK and how many are present
a kinase 4
44
what is STAT and how many are present
a signal transducer and activator of transcription 7
45
What does the TPO pathway result in
platelet formation
46
what does the EPO pathway result in
erythrocyte production(rbcs)
47
what does mutant JAK2 cause
fibrosis in bone muscle
48
how can fibrosis in bone marrow be treated
ruxolitinibs( a JAK2 inhibitor)
49
where is Ras located
on the inner side of the plasma membrane

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