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cell signalling Flashcards

1
Q

why do cells signal

A
  • communicate
  • respond to intracellular changes
  • response to extracellular environment
  • regulate cell behaviour
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2
Q

list the 4 types of cell signalling

A
  1. contact dependant
  2. autocrine/paracrine
  3. synaptic
  4. endocrine
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3
Q

define contact dependent cell signalling

A

= requires direct contact (through gap junctions or signal molecule is bound on the membrane surface)

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4
Q

define autocrine cell signalling

A

release of signals that can travel short distance to target cell

= signal made by cell affecting the same cell

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5
Q

define synaptic cell signalling

A

release of neurotransmitters across synapse to target cell

= exclusively to neurons

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6
Q

define endocrine cell signalling

A

release of hormones into circulatory system to target distant cells

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7
Q

define paracrine cell signalling

A

release of signals that can travel short distance to target cell

= signal made by the cell and affecting another nearby cell

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8
Q

list the three main steps of cell signalling

A
  1. reception = signal molecule binds to receptor
  2. transduction = intracellular signalling proteins
  3. response = effector proteins initiate a response to the signal
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9
Q

effector protein examples

A
  • transcription factors
  • metabolic proteins
  • cytoskeletal proteins
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10
Q

define reception (cell signalling pathway)

A

= a signal molecule (ligand) binds to a receptor of a target cell

  • sometimes receptor change conformation to allow tighter binding
  • if ligands are similar receptor can recognise multiple ligands
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11
Q

4 classes of receptors

A
  1. ligand gated ion channels
  2. G protein-coupled receptors
  3. enzyme-linked receptors
  4. intracellular receptors
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12
Q

define ion channel coupled receptors

A

usually in rapid synaptic signalling

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13
Q

define G protein coupled receptors

A

associate with trimeric G protein

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14
Q

define enzyme coupled receptors

A

have enzyme activity or associate with an enzyme

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15
Q

define transduction (cell signalling pathway)

A

= signal relayed from receptor to effector proteins

  • involves intracellular signalling molecules
  • regulated by molecular switches (switch from inactive to active state via phosphorylation or GTP binding)
  • important for signal amplification, regulation & divergence
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16
Q

what are intracellular signalling molecules

A

= secondary messengers such as cAMP, Ca2+, IP3, DAD

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17
Q

3 times of responses in a pathway

A
  1. timing & persistence: response can be quick or slow & vary in duration
  2. sensitivity & range: response can be triggered by low or high concentration of ligands & may require a threshold
  3. integration & coordination: response may need combination of signal activation & inhibition
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18
Q

how is cell signalling regulated

A
  1. by molecular switches that control on/off state of proteins
  • phosphorylation
  • GTP binding
  1. location
  2. regulated by affinity & specificity of interaction = specific docking sites in intracellular proteins
  3. regulated by positive & negative feedback loops
  4. regulated by adaption to response
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19
Q

define phosphorylation & reverse

A
  1. protein kinase will phosphorylate a protein by adding a phosphate group through the exchange of ATP to ADP = activating the protein
  2. reverse = a protein phosphatase can remove phosphate group deactivating the protein
20
Q

GTP binding & reverse

A
  1. GEFs (guanine exchange factor) will activate the protein by adding GTP = protein switched on

GTPase activating protein can deactivate the protein by removing GTP and exchanging it for GDP = protein switches off

21
Q

how does location regulate cell signalling

A

= cell signalling can only be switched on if all the signalling molecules are assembled at one location

22
Q

what proteins allow intracellular signalling proteins to bind and assemble

A

scaffold proteins which have interaction domains

23
Q

importance of positive feedback loops

A

for prolonging the duration of response

24
Q

importance of negative feedback loop

A

for limiting the intensity of response

25
Q

what does it mean for a cell to adapt to a response

A

prolonged exposure to signal can decrease the response

adaption allows the cells to become more sensitive to small changes in concentration of signals

e.g. removing receptor

26
Q

role of phosphorylated tyrosines

A

act as docking sites for signalling proteins

27
Q

similarities between G protein-coupled receptors

A
  • structure of the receptor

- associate with trimeric GTP binding protein

28
Q

similarities between enzyme-coupled receptors

A
  • structure

- has enzyme activity or associate with enzyme

29
Q

structure of GPCR

A
  • 7 transmembrane

- heterotrimeric (3 subunits)

30
Q

what is bound to G protein when inactive

A

GDP

31
Q

what happens when a ligand binds to Galpha protein

A

Galpha protein exchanges GDP for GTP, then dissociates from complex

32
Q

what are the steps in the cAMP pathway (GCPR)

A
  1. Active Ga protein binds and activates adenylyl
    cyclase enzyme, which in turn catalyze conversion of
    ATP to cyclic AMP (cAMP).
  2. cAMP (secondary messenger) activates other proteins
    – protein kinase A (PKA)
  3. Activated PKA translocate to the nucleus to activate
    (phosphorylate) cAMP response element-binding
    (CREB) transcription factor.
  4. CREB binds to cAMP response element (CRE) to
    promote gene transcription – neuropeptides,
    hormones, neurotrophic factors
33
Q

what are the steps in the PI (phosphatidylinositol) pathway (GCPR)

A
  1. Active G protein activates plasma
    membrane bound phospholipase C (PLC)
  2. PLC (enzyme) converts phosphatidylinositol 4,5
    -biphosphate (PIP2) into inositol 1,4,5-triphosphate (IP3) and diacylglycerol
    (DAG)
  3. DAG activates protein kinase C (PKC) to
    regulate activity of other effector proteins (catalyse/phosphorylate).
  4. IP3 binds IP3 receptors in the ER to regulate Ca2+ concentration
    – regulate
    activity of Ca
    -dependent enzymes (eg. PKC) = postive feedback
34
Q

is the cAMP a slow or fast response

A

slow

35
Q

is the IP a slow or fast response

A

fast

36
Q

what does binding of ligands to receptor tyrosine kinase cause (enzyme linked receptor) & the following MAPK pathway

A
  1. dimerisation
  2. which activates the kinase domains –> phosphorylates tyrosine residues on the receptor
  3. phosphorylation sets off a chain reaction to trigger additional phosphorylation events
  4. phosphorylated sites act as docking sites for other adaptor proteins

MAPK pathway:

  1. Adaptor protein (GRB2) binds receptor
    phosphotyrosine residues at SH2 domain.
    (GRB2 contains SH3 domains that allow
    Sos to bind)
  2. Sos recruits Ras to the complex.
  3. Sos
    promotes GTP exchange for GDP on Ras.
  4. Ras is a family (HRAS, NRAS and KRAS) of GTPase proteins.
  5. Activated Ras
    complex dissociates from Sos, but remains
    bound to the cytoplasmic membrane
  6. Active Ras phosphorylates (activates) Raf proteins (ARAF, BRAF, CRAF,MAPKKK)
  7. Active Raf phosphorylates MEK kinase (MAPKK) - exchange of ATP to ADP
  8. Active MEK phosphorylates ERK
    (MAPK)
  9. Activate ERK can phosphorylate
    other proteins to change protein activity or initiate gene transcription (by inducing transcription pathway)
37
Q

define dimerisation

A

conformational change to bring kinases in close proximity - brings the two monomers close proximity allowing phosphyrlation

38
Q

what is bound to Ras when active compared to inactive

A

Ras functions
as molecular switch
– active = GTP bound,
inactive = GDP bound.

39
Q

what activates the PI3K pathway

A

binding of ligand to RTK

40
Q

role of PI3K pathway

A

cell survive and growth

41
Q

role of phosphatidylinositols (PIs) in PI3K

A

= secondary messenger or docking site for other signalling proteins

42
Q

what happens in PI3K pathway

A
  1. PI3K binds to RTKs and is
    activated. Activated PI3K
    phosphorylate PIP2 to PIP3
  2. PIP3 recruits protein
    kinases AKT and PDK1, bind
    via the PH domains (allow close proximity)
  3. AKT is phosphorylated by PDK1 and mTOR
    complex.
4. Activated AKT further phosphorylates other
target proteins (Bad).
  1. Phosphorylation of Bad results in release of
    apoptosis inhibitory protein, causing inhibition
    of apoptosis
43
Q

what does Wnt/B-catenin signalling regulate

A

cell fate, differentiation & proliferation

In the absence of Wnt ligand, the
Frizzled and LRP receptors at the cell
membrane remain inactive
2. The Dishevelled protein in the
cytoplasm is inactive
3. The destruction complex (Axin, APC,
GSK3, CK1) IS active
4. The destruction complex targets Bcatenin for degradation –
ubiquitinylate, then send to the
proteasome to be broken down
44
Q

steps in Wnt/B-catenin signalling

A
  1. Wnt ligand binds to the Frizzled and LRP receptors at the membrane
  2. Frizzled is activated, recruits and activates Dishelleved at the membrane
  3. LRP recruits and is phosphorylated by
    CK1 and GSK3
  4. Axin binds to phosphorylated LRP and
    destruction complex is disrupted
  5. B-catenin is released, translocate to the nucleus and activate transcription by binding LEF1/TCF transcription factors.
45
Q

the steps in the MAPK signalling pathway

A
  1. RTK gets phosphorylated
  2. GRB2 binds RTK
  3. Sos binds GRB2
  4. Sos recruits RAS
  5. RAS dissociates from Sos
  6. RAF gets phosphorylated
  7. MEK gets phosphorylated
  8. ERK gets phosphorylated
  9. ERK translocate to the nucleus
46
Q

Which protein activates GTPase by stimulating the release of GDP?

A

guanine nucleotide exchange factor

hc (11 decks)

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