Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

The Specialised Cell > Signalling pathways > Flashcards

Signalling pathways Flashcards

1
Q

Beta-1 receptors, myocytes

A

Gs - increase cAMP, increase PKA

Positive isotropy (increased contractility) - increased Ca2+ entry
Po of L-type Ca channels - increased influx
Po of RyR2 - increases Po
Increased [Ca] on every heartbeat - increases contractility

Positive lusitrophy (increased rate of relaxation) - increased Ca removal
Po of PLB (phospholamban) - removes inhibition of SERCA2A (pumps Ca into stores)
Po of troponin I - decreases affinity for Ca, promotes muscle relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Beta-2 receptors, smooth muscle

A

Gs, relaxation
Agonist = adrenaline
Po + inhibits myosin light chain kinase (MLCK)
P-MLCK - decreased affinity for CaM-Ca, cannot Po MLK
Unphosphorylated MLC = important in relaxtion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PKA metabolism

A

Increases metabolism

Po + activates phosphorylase kinase
Activates phosphorylase - important in glycogen breakdown/glycogenolysis

Po transcription factors such as CREB - binds to CRE regions of DNA, stimulates transcription of genes involved in glujconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alpha-1 receptors, smooth muscle cell

A

Gq
Agonist = adrenaline
Smooth muscle cell contraction - vasoconstriction

Activates Ca stores, increases Ca
Ca binds to calmodulin, conformational change

Ca-calmodulin complex binds + activates MLCK
MLCK Po MLC = important in contraction

ie. Salivary gland secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PKC activation

A

Ca binds to C2 region of PKC
cPKC has high affinity for lipids - translocates to DAG in the membrane
DAG binds, removes psedosubstrate motif out of binding site + activates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Exocrine secretion - ie. salivary gland

A

mAChR activates Gq
Ca = exocytosis of amylase-containing vesicles
Ca = activates Ca-activated Cl- channel - efflux of Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alpha-1

A

Gq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Beta-1

A

Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Beta-2

A

Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alpha-2

A

Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alpha-2, smooth muscle

A

Gi
Agonist = adrenaline
Blocks inhibitory pathway - blocks Po of MLCK
Contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Golf GPCR

A

Gs pathway - increases cAMP
Activates cAMP-gated channels
Olfaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gt GPCR

A

Transduction of light

Light - activates GPCR, GTP-bound-alpha subunit activates phosphodiesterase (PDE)
PDE cleaves cGMP –> CMP
No Na+ current - hyperpolarisation

Dark - GPCR not activated
cGMP activates cGMP-gated Na+ channels
Produces dark current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

GIRK channels

A

Inwards rectifying K+ channels
Beta-gamma subunit mediated - Gi

GPCR - beta-gamma subunit activates GIRK channel
Hyperpolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Receptor desensitisation

A
  1. Agonist mediated
    * GPCR Po on the cytoplasmic tail by GRK (G-protein kinase)
    * Po generates binding sites for arresting
    * Arrestin binds - GPCR is internalised
    * Signal stops, arresti detaches, re-inserted into cell membrane
    * Pro-longed signal = internalised receptors in granules fuse with lysosomes + degraded
  2. 2nd-messenger mediated
    * Gs generates PKA
    * PKA Po cytoplasmic tail of GPCR, inactivate signalling
    * Depending on cell type/GPCR - can stimulate internalisation via arrestin binding
  • Gq generates PKC
    Direct: PKC Po cytoplasmic tails of the GPCR
    Indirect:
  • PKC Po + activates GRK, Po tails
  • PKC can Po regulatory proteins, bind to cytoplasmic tail, switch off GPCR signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Receptor tyrosine kinase

ie. RTK (growth factor receptor)

A

Growth factor binds
Dimerisation of receptors, autophosphorylation in the kinase domain, increases tyrosine kinase activity
Phosphorylation sites allow for the recruitment of signalling molecules, Po by the tyrosine kinase activity

17
Q

PIP2

A

PLC, cleaved: PIP2 –> IP3 + DAG

PI3 kinase, phosphorylated: PIP2 –> PIP3

18
Q

SH2 domain

A

src homology domain 2
src = non-receptor tyrosine kinase
SH2 = domain in signalling proteins that can bind to specific phosphorylated residues

19
Q

Small G-proteins

A

Example: Ras, Rho, Rac
Ras mutations leads to tumours (Ras involved in control of the cell cycle)
GEF: stimulate GTP-binding (activate)
GAP: stimulate GTP hydrolysis (inactivate)

20
Q

Adaptor proteins

A

ie. Insulin receptor substrate (IRS)

Insulin binds and activates insulin receptor
Recruitment and phosphorylation of IRS
PI3 kinase has SH2 domains (binds Po proteins) - binds to P-IRS, enables activation of PI3 kinase
PI3 kinase Po lipids (PIP2) in the membrane
PIP2 –> PIP3
PKB is recruited
PKB is phosphorylated + activated by PDK1 kinase- leads to fusion of vesicles containing GLUT4 transporters

21
Q

Sos

A

GEF for Ras - activate Ras

22
Q

MAP kinase pathway

A

Activated downstream of RTKs
Po and activated - recruit Grb-2 (adaptor)
Grb-2 Po and binds to Sos (GEF for Ras)
Activated Ras (binds GTP) activates Raf-1 kinase
Raf-1 Po Mek1/2 kinase
Mek1/2 kinase Po Erk1/2 k
Erk1/2 + Rsk mediates transduction of genes

MAP-K cascades have a mitogenic effect on cells - stimulate growth and proliferation

23
Q

Cytokine receptors

A

Enzyme not intrinsic - associated (coupled) or bound to TK (not intrinsic to the receptor)

JAK-2 binds to cytokine receptor
Cytokine activates receptor - autophosphorylation and activation of JAK-2 kinase
JAK-2 kinase can Po transcription factors such as STATs
Po STATs, dimerise + enter nucleus

24
Q

Cytoplasmic receptors

A

ie. Guanyl cyclase

Receptor in cytosol - ligand must be small + hydrophobic
Peptide bind to receptor
Activates intrinsic guanyl cyclase activity - stimulates an increase in cGMP, activates PKG
Leads to reabsorption of water
(Similar to how cAMP activates PKA)

  • NO released by endothelial cells, bind to cytosolic guanyl cyclase (smooth muscle cells), increase cGMP, activates PLG
25
Q 
Smooth muscle cells
Cytoplasmic receptor (guanyl cyclase)
A

NO released by endothelial cells, bind to cytosolic guanyl cyclase (smooth muscle cells), increase cGMP, activates PLG

Reduce IC [Ca]

  • Po Ca2+ channels - reduce influx
  • Po IP3 receptors (causes Ca release from IC stores) - less sensitive to IP3

cGMP activate PKG

  • Po + activate MLC phosphatase - dephosphorylate MLC (important in relaxation)
  • Po K+ channels leading to hyper polarisation
26
Q

Cortisol receptor

A

Nuclear receptor
Ligand - small + hydrophobic to pass through membrane
Bind + translocate to the nucleus
Regulates transcription

  • Cortisol receptor is bound to a chaperone protein, ligand binds + chaperone is released
27
Q

Only nuclear hormone which binds in the nucleus - does not bind in cytosol + get translocated

A

Thyroid hormone

The Specialised Cell (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions