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Physiology > W2 - Cell to Cell Signalling > Flashcards

W2 - Cell to Cell Signalling Flashcards

1
Q

What is trans autophosphorylation?

A

The molecule phosphorylates itself and then passes that phosphate on

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2
Q

What happens once a GPCR is activated?

A

GTP replaces GDP bound to alpha subunit, alpa/beta/gamma heterotrimer dissociates and alpha dissociates from this

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3
Q

Where does the GTP alpha go after it dissociates and what does this do?

A

Goes to effector protein and activates a cascade to reach target

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4
Q

What are the two forms of direct signalling?

A

Gap junction signalling and juxtacrine signalling

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5
Q

What are the four indirect forms of signalling?

A

Autocrine, paracrine, endocrine and neuronal signalling

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6
Q

In what instance would membrane bound receptors be typically used?

A

When the signal is hydrophilic (except gases)

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7
Q

What happens after transduction if there’s no 2nd messenger or if it’s there but is inactive?

A

Not there - enzyme is activated to produce 2nd M, is there but inactive - changes conformation of enzyme/messenger to activate 2nd M

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8
Q

Ligand and receptor interactions can be fast and/slow, give examples of these?

A

Fast - altering protein function (act/deact), Slow - altering gene expression (takes longer due to transc/transl)

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9
Q

What determines what the head and tail is in a fruit fly?

A

The protein gradients formed by bicoid and nanos proteins

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10
Q

What type of signalling is involved in the formation of chicken limbs?

A

Paracrine

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11
Q

What does the ZPA do?

A

Sends out signals which instruct the developing limb bud on how to form along the posterior/anterior axis

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12
Q

What would give more reference points in terms of ‘decisions made’ by what/how much morphogen are present and why?

A

Having multiple morphogens can give many more combinations to instruct what to produce (e.g. neurons from SC)

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13
Q

How to test French Flag hypothesis

A

Have normal ZPA working and observe, cut ZPA from one embryo using eyelash and add to opposite side (to current ZPA) of another to alter gradients

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14
Q

Wolpert’s conclusion is…

A

A morphogen produces a signalling gradient and this gives identities at thresholds

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15
Q

What is on the X and Y axis of Wolpert’s graph?

A

X - distance from morphogen source, Y - conc of morphogen

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16
Q

What is the difference when writing bicoid mRNA or bicoid protein?

A

mRNA - lowercase and italics, protein - capital letter and upright

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17
Q

What is special about the specificity of serine + threonine kinases and why?

A

Either kinase can phosphorylate either aa because their side chains are similar

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18
Q

Why can kinases only phosphorylate serine/threonine/tyrosine?

A

It requires a polar hydroxyl group on side chain

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19
Q

Why does phosphorylation increase hydrophilicity in serine/threonine/tyrosine?

A

Adds -ve charge so makes side chain charged

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20
Q

What does phosphorylation of tyr/thr/ser do to the structure of protein, allowing it to alter activity of another protein?

A

Conformational change

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21
Q

What enzymes are required for dephosphorylation?

A

Phosphatase enzymes

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22
Q

Are molecules always activated once phosphorylated?

A

No they can be inactivated too

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23
Q

What is the key steps of amplification?

A

One activated receptor activates many 2nd messengers, the 2nd messengers activate multiple kinases until they’re removed from cytosol/metabolised, each kinase can activate multiple targets

24
Q

Amplification can be big or small, is it ever not there?

A

No

25
Q

How do ligand-dependent transcription factors modulate gene expression?

A

Causing addition or removal of acetyl groups from histones

26
Q

Where is the nicotinic acetylcholine receptor found?

A

Neuromuscular junction

27
Q

How many subunits is the NAChR made up of and what happens when the biogenic amine ACh binds?

A

5, conformational change to open aqueous ion channel for movement of K+, Na+ and Ca2+

28
Q

What terminal of transmembrane domains is the ligand binding domain in ionotropic receptors?

A

N-terminal

29
Q

How many transmembrane alpha-helices in a GPCR?

A

7 (always)

30
Q

What two parts of a GPCR makes up site of interaction for G-proteins?

A

3rd intracellular loop and C-terminal

31
Q

What two things can G-proteins interact with once the GPCR is stimulated?

A

Ion channels or enzymes

32
Q

GCPRs can couple many different G-proteins including heterotrimeric Gi/s/q/t/(12/13), what are the three subunits of these?

A

Alpha, beta and gamma

33
Q

When GPCR is bound to, a conformational change occurs, what does this cause to happen?

A

Alpha subunit swaps GDP for GTP

34
Q

What does the active GTP-bound alpha subunit do?

A

Dissociates from beta/gamma and moves along inner surface of membrane until it interacts with an effector protein

35
Q

What in the GPCR signalling pathway generates the active second messenger ion/molecule?

A

The effector protein

36
Q

What 3 things can stop the GPCR pathway?

A

GTPase activity (GDP relaces GTP to inactivate alpha), primary messenger not present or receptor is desensitised to ligand

37
Q

What does Gs and Gi do to adenylyl cyclase? (ATP –> cAMP)

A

Gs - increases rate of activity, Gi - decreases rate of activity

38
Q

How to turn cAMP into 5’-AMP? (stops activating PKA)

A

Cyclic nucleotide phosphodiesterase

39
Q

Gq acts with phospholipase C, what does this enzyme do?

A

Hydrolyses PIP2 to form 2 secondary messenger molecules, DAG and IP3

40
Q

IP3 acts on IP3 intracellular receptors to allow Ca2+ out of ER, what can Ca2+ then act as a 2nd messenger to?

A

CaM kinase, PKC

41
Q

PKC can act on the AP-1 transcription factor, what is this TF used in?

A

Cell proliferation

42
Q

How can the Gq signal pathway be stopped? (2 ways)

A

Hydrolysis of IP3 and moving Ca2+ out of intracellular space

43
Q

In the receptor tyrosine kinases for insulin/IGF, what are the two parts of the receptor dimer joined by?

A

Disulphide bonds between cysteine R groups

44
Q

Once the RTK is bound to, a conformational change occurs which allows for…

A

Phosphorylation of downstream signalling target proteins (e.g. IRS) and transautophosphorylation

45
Q

Phosphorylated IRS can activate PI3K, what is the substrate for PI3K?

A

Membrane phospholipids

46
Q

What type of receptor activity takes place for BMPs and transforming growth factors (beta)?

A

Receptor serine/threonine kinase (RSTK)

47
Q

What proteins do RSTKs phosphorylate and what do the phospho form do?

A

Smad proteins, phospho smads act as TFs and regulate gene expression in nucleus

48
Q

What non-receptor protein kinase enzymes do type I and II cytokine receptors associate with?

A

JAK enzymes

49
Q

On binding the cytokine receptor, dimerisation occurs and then what?

A

JAK enzymes transphosphorylate tyrosine residues in the receptors

50
Q

Through SH2 domains, what do the phosphotyrosines allow to dock onto the receptors? And then what happens?

A

STAT proteins, JAK enzymes phosphorylate the STAT proteins which causes them to dissociate and dimerise with each other

51
Q

What do STAT-STAT dimers act as?

A

They act as TFs once transported into the nucleus

52
Q

What do the enzyme linked receptors for ANPs include instead of kinases?

A

Guanylyl cyclase

53
Q

What happens once the ANP binds to it’s receptor N domain? (vasodilation pathway)

A

Guanylyl cyclase is activated, GTP is made into cGMP and cGMP acts on PKG (ser/thre) to relax smooth muscle in blood vessels

54
Q

What enzyme stops the ANP pathway and how?

A

cGMP-PDE, forms 5’-GMP so it can no longer activate PKG

55
Q

What is an example of paracrine signalling?

A

Mast cells and immune cell recruitment for inflammation

Physiology (14 decks)

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