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Biomed year 2 sem 1 > BMS2002 - cell signalling > Flashcards

BMS2002 - cell signalling Flashcards

1
Q

3 stages of signal transduction

A
  1. reception - EC signal activates membrane receptor
  2. transduction via amplifiers, second messangers, pathways
  3. response
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2
Q

responses from signal transduction

A

transport protein->altered ion transport
metabolic enzyme -> altered metabolism
gene regulatory protein -> altered gene expression
cytoskeletal protein -> altered shape or movement
cell cycle protein -> altered cell growth and division

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3
Q

first messengers are..

A

chemicals that can serve as extracellular signalling molecules

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4
Q

examples of second messengers

A

amines, peptides/proteins, steroids, other small molecules (aas, ions, gasses)

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5
Q

cell surface receptors

A

bind EC molecules -> wide range of IC signal transduction pathways
FAST response

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6
Q

intracellular nuclear recdptors

A

bind molecules that can freely pass membrane by diffusion
often act as transcription factors
SLOW response

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7
Q

4 main classes of receptors

A
  1. ligand gated ion channels
  2. GPCRs
  3. Enzyme-linked
  4. Nuclear
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8
Q

nicotinic acetylcholine receptor

A

ligand gated ion channel
binds Ach -> channel opens -> Na+ in
binds nicotine
electrical event -> response
calcium can also enter

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9
Q

y-amino buytyric acid gabaA receptor

A

ion channel Cl-
inhibitory receptor
activated by benzodiapines, alcohol, anaesthetics

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10
Q

muscarinic acetylcholine receptor

A

indirectly links with membrane ion channels (signal transduction pathways)
more sensitive to muscarine than nicotine

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11
Q

ionotropic receptors

A

form an ion channel pore
e.g. nictotinic Ach receptor, gabaA

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12
Q

metabotropic receptors

A

indirectly linked with membrane ion channels via signal transduction pathways - often g protein mediated

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13
Q

GPCR mechanism

A
  1. unstimulated cell
  2. adrenaline binds beta adrenoreceptor
  3. b adrenoreceptor - G protein interaction
  4. GDP/GTP exchange
  5. alpha subunit liberation
  6. Free a subunit activates AC -> camp -> PKA activation
  7. unbinding of adrenaline/ GTP hydrolysis -> unstimulated cell
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14
Q

cAMP activates

A

PKA

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15
Q

PKA..

A

catalyses transfer of ATP to specific serine/threonie residues on substrate proteins

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16
Q

physiological responses mediated by cAMP/PKA

A

Kidney collecting duct - activated by vasopressin -> water retention
Vascular smooth/cardiac muscle- activated by adrenaline -> relax/increase HR
Colonic epithelium- various factors -> fluid/electrolyte secretion
Pancreas - glucagon-> release of glucose into blood

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17
Q

b-ARK

A

beta adrenoreceptor kinase

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18
Q

steps of desensitization of receptor

A
  1. protein phosphorylation -> cell response
  2. PKA phosphorylates b-ARK -> increases activity
  3. b-ARK phosphorylates b-adrenoreceptor -> reduced affinity for adrenaline
  4. reduced affinity -> reduced cellular response (even if sustained stimulation)
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19
Q

Gs

A

stimulates AC
- couples with b-adrenoreceptors, vassopressin receptor, A2a/B adenosine receptors

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20
Q

Gi

A

inhibits AC
- a2 adrenoreceptors, m & a opiod receptors, A1/3 adenosine receptors

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21
Q

how does cholera toxin target G-proteins

A

cholera toxin activates a s subunit -> ADP dephosphorylation -> conformational change to cause permanent binding to GTP -> constant signalling -> continuous cAMP production
- in colon: activation of PKA-dependent Cl- channels -> lose water and Na+/Cl-
-> secretory diarrhoea

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22
Q

how does pertussis toxin affect g-proteins

A

acts on alpha I subunit -> forces subunit to remain inactive -> prevents activation of AC/PKA -> phosphorylation -> symptoms of whooping cough

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23
Q

Gq pathway

A

Gq stimulates PLC -> cleaves PIP2 into IP3 and DAG
IP3 -> Ca2+ release from ER
DAG-> recruits PKC -> regulates cell shape/proliferation/ transcription factors, mediates desensitization

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24
Q

blood pressure control

A

alpha1- adrenoreceptor -> vasoconstriciton -> increase blood pressure
beta2-adrenoreceptor -> vasodilation -> decrease blood pressure

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25
Receptor Guanylyl Cyclases mechanism of signalling
ANP binds -> receptor dimerization and activation -> generates cGMP -> activates other signalling molecules
26
Receptor serine/threonine kinases mechanism of signalling
first messenger binds to receptor type 2 -> receptor 1 then binds, forms complex with all three units -> type 2 phsphorylates type 1 -> activates ser-thr kinase activity of type 1 -> type 1 phosphorylates target proteins
27
Receptor tyrosine kinases (RTK) mechanism of signalling
binding of two insulin molecules -> receptor dimerises -> phosphorylate eachother -> creates phosphotyrosine motifs -> recruit intracellular signalling molecules
28
Tyrosine kinase-associated receptor mechanism of signalling
first messenger binds -> dimerization of the receptor -> activation of tyr kinases -> these phosphorylate tyr residues on themselves and on the receptor -> these motifs recruit intracellular molecules
29
Receptor tyrosine phosphatase mechanism of signalling
CD45 binds -> activates tyr phosphorylase activity -> dephosphorylates target protein -> regulation of downstream cell-signalling events
30
how is glucose stored?
as glycogen, mostly in muscles and liver
31
after a meal
increased glucose absorption -> increased glucose conc in circulation -> can stimulate metabolism and increase o2 demand abundant glucose stored as glycogen
32
between meals
absorption is minimal -> reduced glucose conc -> may limit metabolism and reduce o2 demand
33
pro-insulin
converted by prohormone convertase -> removes C peptide -> left with 2 polypeptide chains held by disulphide bridges
34
two phases of insulin secretion
first: release of insulin stored in secretory granules (rapid, transient) second: synthesis and secretion of new insulin (slower, sustained)
35
insulin circulates..
freely - v little plasma protein binding
36
insulin is degraded by
insulinase, mainly in liver/muscle/kidneys
37
Glucose transporters on beta cells
GLUT2 - system is hormone-insensitive (always active) - glucose -> ATP
38
beta cells K+ channels
ATP sensitive - open at normal levels, closed at very high levels of ATP -> control membrane potential -> external glucose can set membrane potential
39
beta cells VG Ca2+ channels
- opened by depolarisation -> makes cells permeable to calcium -> depolarisation increases membrane permeability to Ca2+
40
Beta cell exposed to normal glucose
normal glucose -> normal internal ATP -> K+ channels open -> Vm is hyperpolarised -> Ca2+ channels closed -> b cell doesnt secrete insulin
41
beta cell exposed to high glucose
high glucose -> high internal ATP -> K+ channels close -> depolarised Vm -> Ca2+ channels open -> b cells secrete insulin
42
insulin is released from the (1) into the (2)
1. pancreas 2. hepatic portal vein
43
insulin receptors
dimeric: alpha and beta subunits - insulin binding -> dimerization -> activation - receptor dimerises -> subunits phosphorylate eachother at multiple tyrosine residues
44
insulin receptor signalling
insulin binds receptor -> receptor dimerization + activation -> receptor phosphorylates IRS-1 -> P13K activation -> cellular responses to insulin
45
insulin promoting glucose uptake by liver
insulin induces P13K activation -> P13K activates PKB -> induces translocation of GLUT4 to plasma membrane -> GLUT4 allows glucose entry
46
insulin promoting glycogen synthesis
insulin activates PKB -> activates GSK-3 -> activates glycogen synthase -> glycogen synthesis
47
insulin promotes fat deposition in adipocytes
insulin allows glucose into cell via GLUT4 -> glucose metabolised to glycerol - insulin inactivates lipase - excess fatty acids in the cell
48
insulin promotes synthesis of new proteins
insulin receptor -> P13K -> TORC1 -> protein synthesis - when amino acids are abundant, insulin stimulates their incorporation into proteins
49
2 things that promote insulin release
1. hyperglicemia 2. raised levels of amino acids
50
4 effects of insulin
1. promotes uptake and storage of glucose 2. promotes metabolic utilisation of glucose 3. promotes storage of fat 4. promotes synthesis of new protein
51
glucagon is secreted by (1) in response to (2)
1. pancreatic alpha cells 2. low glucose concentration
52
glycogenolysis
glucose release from liver
53
glycogenolysis signalling pathway
glucagon activates AC -> cAMP activates PKA -> activates phosphorylase kinase A -> phosphorylase A (adrenaline can also activate this pathway by b-adrenoreceptors)
54
gluconeogenesis
glucose formation from lipids and amino acids stimulated by glucagon
55
3 things that stimulate glucagon release
1. hypoglucemia 2. vigorous exercise 3. raised levels of amino acids
56
3 effects of glucagon
- glycogenolysis - gluconeogenesis - ketogenesis
57
Diabetes mellitus
inability to regulate blood glucose
58
blood sugar levels in diabetes
>7mM (5mM is normal)
59
pathogenesis of T1DM
environmental factors/genetic predisposition -> autoimmune destruction of beta cells (CD8+ mediated) -> severe insulin deficiency -> hyperglycaemia
60
genes associated with T1DM
HLA-DR3/DR4
61
no insulin ->
glucose not used as metabilic fuel -> rapid weight loss -> fatty acids -> ketone bodies -> decreased pH -> metabolic acidosis -> acidic coma
62
hyperglycemia and dehydration
high conc of glucose enters glomerular filtrate -> overwhelms PCT glucose absorbing capacity -> increases fluid osmolarity in tubules -> more water secreted from cells into PCT -> water reabsorption is reduced -> urine flow is increased -> dehydration, excessive urine production, thirst
63
problems with injecting insulin therapy
- exogenous insulin into general circulation, natural insulin into portal circulation - lipohypertrophy (fat deposition around repeated injection site as insulin promotes fat deposit) -> unpredictable rate of insulin absorption
64
soluble insulin
rapid/short lived IV in emergencies
65
isophane insulin
intermediate acting tends to form precipitates
66
insulin zinc suspension
long acting tends to form precipitates
67
insulin lispro
insulin analogue v. rapid/short lived normally taken before a meal
68
insulin glargine and detemir
insulin analogue long acting, slowly absorbed normally taken before a meal in combo with short-acting forms a micro-precipitate at physiological pH
69
teplizumab
drug to target autoimmune reaction in diabetes type 1
70
pathogenesis of T2DM
1. genetic and environmental predisposition (lifestyle, obesity) 2. insulin resistance 3. hyperinsulinemia -> beta cells try to compensate for peripheral resistance 4. beta cells fail to keep up -> hypoinsulinemia 5. diabetes: total failure of insulin
71
diabetes 2 and free fatty acids (FFA)
excess FFA are transformed into DAG -> activate PKC -> phosphorylate IRS-1 -> attenuates insulin receptor signal -> insulin resistance in muscle and liver
72
diabetes 2 and adipokines
released by adipocytes can be pro- or anti-hyperglycaemic adiponecting (anti-hg) is reduced in obesity
73
diabetes 2 and inflammation
adipocytes produce IL-6 and IL-1 -> attract macrophages to fat deposits reduction of cytokines can improve insulin sensitivity
74
diabetes 2 and PPARy
nuclear receptor involved in adipocyte differentiation, promotes secretion of anti-hyperglycemic adipokines mutations cause diabetes
75
Thiazolidinediones for T2DM
PPARy agonist promotes secretion of anti-hyperglycaemic adipokines -> increases lipolysis sensitize cells to insulin collectively reduces insulin resistance in liver/perpheral tissues
76
Metformin for T2DM
supresses glucose release from liver activates AMPK increase lipolysis in muscles and liver -> improve insulin receptor signalling suppress glucose release from liver
77
Sulphonylureas for T2DM
bind sulphonylurea receptors on beta cell membranes block ATP sensitive K+ channels on b cells -> K+ accumulates insise -> cell depolarises -> Ca2+ channels open -> allow insulin secretion y exocytosis
78
macro complications of T2DM
hyperglycemia -> macrovascular disease -> damage to medium/large blood vessels -> coronary heart disease, cerebrovascular disease, peripheral vascular disease
79
micro complications of T2DM
hyperglycemia -> microvascular disease -> damage to small blood vessels -> retinopathy, nephropathy, neuropathy
80
ROS generation
from excess glucose and FFA -> micro- and macro-vascular complications of T2DM
81
AGE generation
from excess sugar molecules and proteins -> vessel damage
82
AGE effect on blood vessels
AGE crosslinks with collagen -> basal membrane of endothelium thickens -> traps LDL and IgGs -> oxidation, complement activation, inflammation -> vessel damage

Biomed year 2 sem 1 (7 decks)

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