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Cells > Mod7 - Cell Response to the Environment > Flashcards

Mod7 - Cell Response to the Environment Flashcards

1
Q

What are the two (most) general categories of signals?

A

Signals generated by cell-cell contact; signals generated by free diffusion of ligands

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2
Q

Describe what happens in signalling by cell-cell contact

A

There is no release of secreted molecules; the receptor and signal molecule are both bound to/in the plasma membrane

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3
Q

Which kind of cell signals CAN cross the cell membrane?

A

Small, hydrophobic signal molecules that bind INTRAcellular receptors

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4
Q

What happens after signal molecules bind intracellular receptors?

A

Usually, this causes a conformational change in the receptors, which activates it, and causes it to translocate to the nucleus where it activates or represses transcription of a gene

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5
Q

How is specificity achieved in intracellular signalling?

A

There is specificity in both the Ligand-Receptor interaction (steroid binding domain) and the Receptor-DNA interaction (DNA-binding domain)

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6
Q

What kind of signal molecules cannot cross the cell membrane?

A

Large, hydrophilic molecules (e.g., proteins)

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7
Q

What is meant by paracrine signalling?

A

Diffusion of signals over a SHORT distance to target neighbouring cells (e.g., Epidemial Growth Factor EGF)

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8
Q

How does neuronal signalling occur (e.g., distal/local)?

A

Strictly local between two cells (signal released into synaptic cleft, e.g., Acetylcholine)

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9
Q

How does endocrine signalling occur? (E.g., remote/local)

A

REMOTE signals act over the whole body via the blood stream to target cells (e.g., insulin, adrenaline)

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10
Q

How is acetylcholine an example of “1 signal -> 2 responses”

A

It causes contraction in skeletal muscle cells, but decreased rate and force of contraction in heart muscle cells

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11
Q

What are the three main general categories of cell surface receptors?

A

Ion-channel-coupled receptors; G-protein coupled receptors; Enzyme-coupled receptors

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12
Q

What is the common structure of all GPCRs?

A

7 transmembrane spans across the lipid bilayer - 3 loops facing the Extracellular Space, 3 facing Cytosol, and the C-terminus facing the cytosol

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13
Q

What activates GPCRs (and 4 examples)?

A

Extracellular ligands (e.g., glucagon, histamine, adrenaline, dopamine)

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14
Q

What inactivates GPCRs?

A

Phosphorylation and internalisation

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15
Q

How do GPCRs allow extracellular signals to affect the cell?

A

The ligand binds to the receptor, causing a conformational change, which is then “transferred” to the coupled G-protein;
the G-protein acts as a molecular switch to activate an effector, or GAP (GTPase-Activated Protein)

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16
Q

What are the three subunits called in trimeric G proteins (and which two are actually anchored to the membrane)?

A

alpha, beta and gamma (alpha and gamma)

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17
Q

What happens to a trimeric G protein when it is activated?

A

It dissociates into the alpha subunit, and the ß-gamma complex

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18
Q

How is GTP->GDP hydrolysis affected by the activation of the effector?

A

Once the G-protein interacts with the effector, hydrolysis to GDP is ENHANCED

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19
Q

What are the usual targets of trimeric G-proteins?

A

Ion channels or membrane-bound enzymes (the products of these enzymes act as second messengers)

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20
Q

What is a “second messenger”?

A

A rapidly produced, diffusible signalling molecule that activates effector proteins (and is rapidly inactivated).

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21
Q

What is the purpose of amplification in signal transduction?

A

To achieve a STRONG activation in a SHORT time

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22
Q

How is the termination of signalling achieved for GPCRs?

A

Endocytosis of the receptor, triggered by phosphorylation of its intracellular domain (inactivation)

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23
Q

What are the two possibilities after a GPCR is inactivated by endocytosis?

A

Degradation or Recycling - if recycled, it can be reactivated quicker than if it is degraded (this decision is regulated by other regulatory events)

24
Q

How is cAMP produced as a second messenger?

A

Once activated by the alpha subunit of the G-protein, The Enzyme Adenylyl Cyclase converts ATP into cAMP

25
Q

What enzyme rapidly inactivates cAMP (and what molecule does it then become)?

A

A phosphodiesterase (just AMP)

26
Q

What does cAMP activate, and what type of enzyme is this?

A

Protein Kinase A (a serine-threonine protein kinase)

27
Q

How does cAMP activate PKA?

A

2 cAMP bind to each of the two regulatory subunits, causing dissociation of the 2 catalytic subunits, so they can be active. (The 2 regulatory subunits are covalently bound to each other, and remain so)

28
Q

How does cAMP production cause amplification?

A

Once cAMP activates PKA, PKA phosphorylates other proteins, which then produce many new intracellular molecules

29
Q

Sorry about some of these flashcards, I know they can be a bit hefty

A

Saul Goodman

30
Q

How does Phospholipase C produce signal molecules (and how is this activated)?

A

It is activated by a GPCR, and then cleaves PIP2 into IP3 (inositol 1,4,5-triphosphate) and DAG (diacylglycerol)

31
Q

What is the general function of phospholipase C(s)?

A
  • Involved in cleavage of membrane phospholipids (e.g., phosphatidylcholine, phosphatidylinositol)
  • Hydrolyse phosphorylated forms of PI (e.g., PIP2 -> PIP -> PI)
32
Q

What are the three main groups of Phospholipase C(s) - and how are they activated?

A

PLCß = activated by GPCRs
PLC(gamma) = activated by RTKs
PLC(delta) = present in cytoplasm

33
Q

How do the products of phospholipase C hydrolysis vary?

A

DAG is always a product, but the other product can be IP, IP2, IP3

34
Q

Once DAG and IP3 are produced by hydrolysis, what is the function of DAG?

A

DAG recruits Protein Kinase C (PKC) to the membrane (localisation)

35
Q

Why is Protein Kinase C not immediately active after membrane localisation by DAG?

A

It also needs Ca2+ (activated by 2 distinct events, unlike PKA+cAMP)

36
Q

Once DAG and IP3 are produced by hydrolysis, what does IP3 do?

A

IP3 binds to a receptor at the Endoplasmic Reticulum, causing CALCIUM (Ca2+) to be released, which then binds to PKC and activates it

37
Q

What are the two other groups of PKC besides convential PKC called?

A

Novel PKC (group B) and Atypical PKC (group C)

38
Q

What is different in structure and function about novel and atypical PKC, compared to conventional?

A

Novel: missing C1, so calcium-independent
Atypical: missing C1 and part of C2, so calcium-independent and Phospholipid-insensitive

39
Q

What is the other (mentioned) example of calcium as a regulator in the cell?

A

Calmodulin:
“Signal” -> increased Ca2+ -> binds to calmodulin -> activates Ca2+/calmodulin=dependent protein kinase (CaMK) -> target protein

40
Q

Which three amino acids are the target of phosphorylation?

A

Serine, Threonine, Tyrosine

41
Q

What is the largest group of Enzyme-Coupled Receptors?

A

Receptor Tyrosine Kinases (RTKs)

42
Q

How are RTKs generally activated, and how do they phosphorylate target proteins?

A

They are activated by a signal molecule in the form of a dimer, bringing the intracellular kinase domains in contact (i.e., stabilising the RTK as a dimer); they then phosphorylate each other on multiple tyrosines to activate

43
Q

How do the tails of RTKs assemble an intracellular signalling compelx?

A

Phospho-tyrosine residues create specific binding (docking) sites to allow association (and activation) of downstream signalling proteins

44
Q

What two ways can RTKs be inactivated?

A
  1. Phosphate removal by Protein Tyrosine Phosphates
  2. Receptor Internalisation (endocytosis and degradation in the lysosome)
45
Q

What is RAS, and how is it related to RTK?

A

It is a monomeric G protein that acts as a molecular switch DOWNSTREAM of RTK, at the plasma membrane

46
Q

What are the two other proteins besides RTK and RAS that are involved in RAS activation?

A

GRB2 (adaptor protein) and SOS (GEF)

47
Q

How does RAS inactivation occur, and what is this catalysed by?

A

GTP hydrolysis to GDP (RAS-GTPase-Activating-Protein, e.g., p120GAP)

48
Q

How does GRB2 (the adaptor protein) interact with the RTK in the RAS activation pathway?

A

SH2 domain binds to phospho-tyrosine residues (Y-O)

49
Q

How does SOS interact with GRB2 in the RAS activation pathway?

A

SH3 domain interacts with proline-rich sequences on GRB2

50
Q

How does SOS activate RAS (and what does NOT occur in this activation)?

A

SOS is a GEF, so GDP is exchanged for GTP, activating RAS (NO direct binding or phosphorylation of RAS)

51
Q

State the stages of the MAPK signalling pathway

A

Activated RAS protein activates MAP kinase kinase kinase;
Which activates MAP kinase kinase;
Which activates MAP kinase;
Which causes changes in protein activity and gene expression

52
Q

What are the three main examples of the roles of MAPK-mediated phosphorylation in the cell?

A
  1. Altered cell metabolism/response to stimuli (Phos. of enzymes)
  2. Altered cell shape (Phos. of cytoskeletal proteins)
  3. Altered expression of genes involved in survival, proliferation, migration and differentiation (Phos. of gene regulatory proteins)
53
Q

What is PI3K?

A

Phosphatidylinositol-3-kinase; a heterodimeric lipid kinase which phosphorylates phospholipids

54
Q

What are the two subunits of P13K, and what are their features?

A

Regulatory subunit (p85 alpha/beta/gamma) -> contains an SH2 domain
Catalytic subunit (p110alpha/beta) -> ATP binding site, dual specificity (phosphorylates inositol lipids AND its associated p85 regulatory subunit at Ser608)

55
Q

What does P13K actually (sort of?) do, and how is this activated?

A
  • Y-P (on the activated RTK) recruits the regulatory subunit of P13K, which recruits the catalytic subunit to the plasma membrane
  • The catalytic subunit converts PIP2 to PIP3, which then recruits PDK1, which activates AKT, PKC, etc.
56
Q

Remember - cell signalling is a COMPLEX BUT CO-ORDINATED NETWORK, with CROSS-TALK

A

thumbs up

cool beans

Cells (8 decks)

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