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BMS2002 > strand 3 > Flashcards

strand 3 Flashcards

1
Q

intracellular signalling

steps?

A
  1. extracellular signal molecule activates membrane receptor
  2. intracel molecules transduced via pathway
  3. cellular response activated

1st messenger (extracellular) 2nd messenger (intracellular) transducers (membrane proteins)

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2
Q

high blood sugar response?

A

insulin release from pancreas (beta islets)

insulin> tissue for glucose conversion to glycogen

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3
Q

low blood sugar response

A

glucagon release from alpha islets in pancreas

glycogen > glucose

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4
Q

types of response

A

altered: ion transport/ metabolism/ gene expression/ cell shape/ movement/cell growth/ division

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5
Q

receptor locations

response speed?

A

cell surface (fast response)
intracellular/ nuclear (slow response)

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6
Q

cell surface receptor molecules

membrane crossing?

pathways?

A

for hydrophilic signalling molecules

can’t cross membrane therefore must bind

variety of pathways

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7
Q

intracellular / nuclear receptor molecules

membrane crossing

responses?

A

hydrophobic molecules

cross PM via simple diffusion

txn factors

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8
Q

4 main receptor classes

A

ligand-gated ion channels (ionotropic)
G-protein coupled receptors (metabotropic)
enzyme-linked receptors
nuclear receptors

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9
Q

3 types of cell surface receptors

A

ligand gated ion
G protein coupled
kinase-linked

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10
Q

ionotropic receptor examples

A

nicotinic ACh receptor
gabaA (gamma-amino butyric acid)

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11
Q

nicotinic ACh receptor

A

mediated ACh effect on muscle
ACh binding opens channel/ allows Na+/Ca+ entry
binds nicotine

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12
Q

GABAa receptor

activators? ion selection? role?

A

activated by GABA (CNS neurotransmitter)/ benzodiazepines
Cl- ion selectivity
role in CNS
inhibitory receptor

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13
Q

metabotropic receptor

example?

A

indirect link w ion channels on PM via signal transduction

e.g. Muscarinic ACh receptor/ GABAb

role in cell function regulation

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14
Q

Muscarinic ACh receptor

A

favour muscarine over nicotine

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15
Q

GABAb

A

activate potassium channels

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16
Q

no. transmembrane domains/ polypeptide chains of metabotropic

no. sub-units per polypeptide chain?

A

7 transmembrane domains
3 polypeptide chains (alpha beta and gamma)

alpha (16) beta (5) gamma (11)

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17
Q

metabotropic polypeptide structure

A

beta and gamma bind tightly to each other (Bgamma subunit)
alpha has guanine nucleotide site binding GTP/GDP

complexes in PM

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18
Q

alpha GTP/ GDP affinity for beta gamma sub-unit

A

alpha GTP> High affinity
alpha GDP> low affinity

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19
Q

G protein cycle

A
  1. adr binds beta-adrenoreceptor
  2. g protein interaction
  3. GTP/GDP exchange
  4. a sub-unit liberation
  5. AC activation
  6. adr unbinding/ GTP hydrolysis
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20
Q

what does cAMP activate

structure of protein activated?

A

PKA (protein kinase A)

2 polypeptide chains (C catalytic and R regulatory)
bound together when

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21
Q

PKA C and R polypeptide chain sub-units

A

2R and 2C form tetramer
R has 2 cAMP binding sites> allows sub-unit dissociation, activation and phosphorylation of other proteins

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22
Q

PKA function

A

catalyzes transfer of serine/ threonine res on substrate proteins

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23
Q

physio responses mediated by cAMP/PKA

A

kidney collecting duct
vascular smooth muscle
colonic eipthelium
pancreas

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24
Q

termination of signal transduction

A

removal/ inactivation of: signal/receptor, signalling proteins, 2nd messengers
dephosphorylation

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25
Q

removal of second messengers

A

cAMP hydrolysed by phosphodiesterase/ unbound from R ^affin C

tetramer reassembly

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26
Q

PDE inhibition

A

caffeine prolongs cellular response

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27
Q

receptor desensitization example

A

beta adrenoceptor kinase
1. PKA phosphorylates BARK ^ activity
2. BARK phosphorylates beta adrenoceptor decreasing adrenaline affin and therefore response

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28
Q

PKA and CREB

A

PKA phosphorylates CREB and activates txn of target genes

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29
Q

G protein sequence

A

G > adenlyl cyclase> cAMP> activated PKA

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30
Q

types of G protein

A

GS
G1
Gq

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31
Q

dual control of adenlyl cyclase

A

alpha s stimulates AC
alpha i inhibits AC

a(s) GTP bound

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32
Q

beta adrenoreceptors

(vasopressin receptor)

A

A(2a/b)> adenosine receptors couple Gs

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33
Q

alpha 2 adrenoceptors

mu/ delta opioid receptors

A

A1/3 couple to Gi

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34
Q

cholera toxin target

where does this occur

A

alpha s sub-unit

causes ADP ribosylation/ prevents GTP hydrolysis

occurs in colon in PKA-dependent Cl- channels (CFTR)&raquo_space; diarrhoea

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35
Q

pertussis toxin target

where does this occur?

A

locks alpha i into inactive config> no receptor activation/ inhib control of AC

in airway (whooping cough)

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36
Q

Gq

sub-units?? activating target?

how does it affect ACh

A

contains alpha(q11)
allow hormones/neurotrans to activate PLC

underlies autonomic ACh effects

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37
Q

PLC

action?

A

Phospholipase C
amplifier enzyme

cleaves PIP2 (membrane phospholipid)

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38
Q

autonomic effects of ACh

why?

A

H1 receptor responses (GI smooth muscle contraction)

due to ^Ca2+

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39
Q

PIP2 cleavage products

A

> IP3 + DAG

Inositol 1,4,5-phosphate + diacylglycerol

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40
Q

IP3 action

characteristic enabling action

A

water-soluble so travels through cytosol to stimulate Ca release from ER

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41
Q

DAG action

characteristic enabling action

A

hydrophobic therefore stays in membrane and recruits PKC

^Ca2+-dependent protein kinase

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42
Q

Calmodullin

complex action?

A

Ca binding protein
each binds 4 Ca2+

Ca2+-CaM complex activates PDE/ CaM kinases

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43
Q

CaM kinase action

A

phosphorylate ser/thre on substrate proteins
smooth muscle contraction

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44
Q

example of Gq coupled receptor

action?

A

alpha 1 adrenoreceptor

^ intra free Ca2+ and activate CaMKs

causes vasoconstriction

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45
Q

DAG

A

Ca2+ dependent PKA
^cell response w phosphorylation ^PKC
mediates BARK densensitisation
regulates: cell shape/ proliferation/ txn factor activity

PKC mediates IPC

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46
Q

alpha 1 adrenoreceptor

A

vasoconstriction via Gq

Gq> PLC>IP3>CaMK

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47
Q

muscarinic receptors

G protein involvement/ no. sub-types?

A

Gq/Gi coupled
ACh activated (metabotropic)
5 sub-types (1,3,5 Gq-coupled) (2,4 Gicoupled)

autonomic ACh effects

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48
Q

enzyme linked receptors examples

A

guanlyl cyclases
tyrosine/serine/threonine kinase
tyrosine phosphatase
tyrosine kinase assoc.

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49
Q

receptor guanlyl cyclase

A

2 guanlyl cyclase domains

convert GTP>cGMP

cGMP activates downstream kinases

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50
Q

guanlyl cyclase mechanism

A
  1. ANP binding (dimerisation/ activation)
  2. guan cyc generates cGMP
  3. other signalling molecules activated

e.g. response of vasodilation

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51
Q

beta 2 adrenoreceptors

A

vasodilation

via Gs>cAMP>PKA

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52
Q

serine/ threonine kinases

A

domains target proteins

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53
Q

serine/ threonine kinase mechanism

A
  1. 1st messenger binds tII receptor
  2. TI binds (ternary complex w TII/1st messenger)
  3. TII phosphorylates TI (activting TI kinase)
  4. TI phosph target proteins

e.g. response of cell proliferation

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54
Q

receptor tyrosine kinases

A

domains phosphorylate selves/ other proteins

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55
Q

receptor tyr kinase mechanism

A
  1. binds 2 insulin molecules (receptor dimerization)
  2. cytoplasmic tyr kinase phosp each other at tyr res (phosphotyrosine motifs)
  3. motifs recruit intra signalling molecules (response)

e.g. insulinmediated glu uptake
MAP kinase signalling pathway

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56
Q

MAP kinase pathway

A
  1. activated Ras protein phosphorylates MAP kinase *3
  2. 4 proteins produced (X,Y > activity change /txn reg A,B >gene exp change)
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57
Q

tyrosine kinase associated receptors

A

non-covalently association w cyto domains

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58
Q

tyrosine kinase associated receptor mechanism

A
  1. 1st messenger binds receptor> dimerization
  2. tyr phos on selves/ receptor (phosphotyrosine motifs)
  3. motifs recruit intra signal molecules
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59
Q

tyrosine phosphatase receptor

A

domains dephosphorylate target proteins

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60
Q

tyrosine phosphatase mechanism

A
  1. CD45 binds receptor
  2. target dephosph by tyr phosp
  3. downstream cell-signalling event regulation
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61
Q

GPCR sequence

A
  • activate intra signal via G> conform change> intra^>signa,lling cascade

2nd messengfer system (cAMP/IP3/DAG)
no enzyme

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62
Q

RTK sequence

A

ligand binding> ^kinase activity> tyr phosph self/downswtream

SH2 domains/ Ras/ MAP kinase/ PI3
direct phosphorylation
enzymatic activ

63
Q

circulating glucose concentration

A

~5mM

64
Q

types of islets of Langerhan

percentages of each/ products

A

alpha (15-20%) > glucagon
beta (65-80%)>insulin
gamma (3-10%)> somatostatin

65
Q

insulin
structure?

inactive form?

A

polypeptide hormone processed in golgi
2 polypep chains held by disulfide bridges (A> 21aa B> 30aa)

pro-insulin is inactive form

66
Q

pro-insulin activation

A

prohormone convertase 1/2 remove C chain of 33 aa

67
Q

insulin storage

A

secretory granules of beta cells w pro-insulin/ c peptide

68
Q

2 phases of glucose infusion against insulin production

A
  1. rapid transient response
  2. slower sustained response

- phase 1: insulin release from secretory granules
- phase 2: synthesis/

69
Q

insulin circulation and degradation

A

circulated in free form
degraded by insulinase

degradation in liver/muscles/kidney

70
Q

plasma half-life

A

~6 mins

71
Q

C chain

A

stable
assayed to indicate insulin secretion

72
Q

insulin and glucose concentration relations

experiments

A

continuous glucose infusion

max insulin when [glu]>9mM

73
Q

glucose transport into beta cell

A

beta cell express GLUT2 transport system

hormone insensitive therefore always active

74
Q

glucose production of ATP/ADP

A

glucose phosphorylated to glucose-6-P (via glucokinase) / metabolized by glycolysis/ mito oxidation > ATP/ADP

in beta cell

75
Q

what is concentration of ATP produced affected by?

A

circulating glucose conc
(also affects intracellular glucose conc)

76
Q

beta cell channels

A

ATP-sensitive K+ channels
v-gated Ca2+ channels

ATP sensitive K+= drug target for diabetes

77
Q

ATP-sensitive K+ channel

opening/ closing

A

open at normal [ATP]
close at high [ATP]

78
Q

v-gated Ca2+ channels

A

close at normal Vm
depolarization opens v-gated Ca2+ channels / ^membrane permeability to Ca2+

cell membrane impermeable to Ca2+

79
Q

normal glucose concentration sequence

A

normal [glu]> normal ATP> K+ open> Vm hyperpolarised> Ca2+channels close> no insulin secretion

80
Q

high [glu] sequence

A

^[glu]> ^ATP>K+close> Vm depolarised> Ca2+ open> beta cell secretes insulin

81
Q

insulin release from pancreas

A

into hepatic portal vein
liver exposed to insulin
portal circulation gut to liver

82
Q

insulin receptor

A

2 sub-units (alpha/beta)

insulin binding ^ receptor dimerization/ activation

dimerization entails phosphorylation of each other at multiple tyrosine res

83
Q

beta sub-units

A

960> substrate binding
1146/1150/1151> phosphorylation
1293/1294/136> atenuates kinase activity
1316/ 1322> ass. w growth signal

84
Q

insulin receptor signalling

A
  1. insulin binding > dimerization
  2. IRS-1 phosphorylation> ^PI3K/ MAPK cascade
  3. PI3K > insulin cellular response

MAPK cascade> cell growth and survival

85
Q

GLUT4

A

intracellular membrane in unstimulated cells

not PM

86
Q

insulin activation of PI3K

> activating protein kinase B

A

evokes translocation of GLUT4 to PM

allows glucose uptake into hepatocyte

87
Q

PKB action

A

phosphorylates/ inhibits GSK3> inhibits glycogen synthase

glyc synthase catalyzes glucose addition to glycogen chain

THEREFORE PIK3 ^PKB which ^GLYCOGEN SYNTHASE

88
Q

Where does glycogen synthase action occur

A

liver/ skeletal muscle

(and all cells but less so)

if glycogen stores are full > glucose> fatty acids in circulation for fat storage

89
Q

brain’s only energy source

A

glucose
(no fatty acids)

90
Q

action of hormone-deprived fat cell

A

low permeability to glucose
fatty acid release to fuel metabolic processes
hormone sensitive lipase breaks down fat

91
Q

insulin supplies adipocyte action

A

high permeability to glucose > metabolised to glycerol and synthesised to fat
insulin inactivated lipase >
excess fatty acids

92
Q

insulin promotion of protein synthesis

A
  1. ^ circulating amino acid conc ^ beta insulin release
  2. insulin receptors ^TORC1
  3. Protein synthesis regulation

insulin receptor>PI3K>TORC1> Protein synthesis

93
Q

TORC 1

A

Target of Rapamycin complex 1

2nd PI3K-dependent kinase

94
Q

what happens when amino acids are abundant

A

insulin stimulates protein incorporation to protein

95
Q

glucagon structure

A

single pp chain
29 aa

hypoglycaemia > glucagon release
hyperglcaemia> glucagon suppression

no glucagon receptor on skeletal muscle cells

96
Q

glucagon receptor

A

G-protein coupled receptor
7 transmembrane domains
couple to Gs
activate lipase

^cAMP/ PKA dependent pathway

adrenaline can also activate via beta adrenoreceptors

97
Q

amino acid effect on insulin/ glucose

A

aa ^insulin/glucagon

^insulin > ^ aa uptake and decrease plasma glucose
^glucagon ^plasma glu

98
Q

gluconeogenesis

A

glucose formation from lipids/ aa

99
Q

diabetes blood glucose concentration

A

> 7mM

hyperglycaemia!!!

100
Q

T1 diabetes

A

insulin secretion failure

low [insulin] high [glucose]
sudden young onset
~5%

101
Q

type 2 diabetes

A

insulin resistance

insulin in circulation but ^[glucose]
obesity assoc. later in life

102
Q

T1 pathogenesis

A

autoimmune beta cell destruction via CD8 Cyto T

103
Q

autoimmune beta cell destruction

A

CD8 reactive against insulin peptides/ MHC complexes
recognized by cytotoxic T lymphocytes

associated w HLA-DR3/DR4

104
Q

hyperglycaemia effect on urinary system

A

^[glucose] in glomerular filtrate ^fluid osmolarity in tubuless
more water into PCT ^urine flow
decreases water reabsorption

105
Q

hyperglycaemic acidotic coma

A

more fat broken down as no glucose for fuel
more fatty acid > lower pH
metabolic acidosis

106
Q

prediction of glucose values

A

glycosylated Hb used to predict gluc values of past 6-8 weeks

107
Q

lipohypertrophy

A

fat deposit around injection site subject to ^[insulin]

negative effect of exogenous insulin injection

108
Q

side effects of insulin therapy

A

lipohypertrophy
unpredictable rate of insulin absorption

109
Q

insulin forms used for therapy

A

animal insulin (Porcine/bovine)
human insulin
human insulin analogue

110
Q

types of human insulin

A

soluble (rapid/ short-lived/ IV emergency)
isophane (forms ppt/ intermediate acting)
insulin Zn suspension (forms ppt/ long-lasting)

111
Q

insulin analogues

A

lispro (Lys28> Pro29/ rapid/ short)
glargine and detemir (long/ micro-ppt at physio pH at subcut/ slow absorption)

112
Q

teplizumab

A

targets autoimmune reaction in diabetes 1

113
Q

hyperinsulemia

hyperinsulemia

A

beta compensate for peripheral resistance > exhausted and decrease secretion

114
Q

free fatty acids

> insulin resistance in muscle/liver

A
  1. transformed in 2nd messeger DAG
  2. DAG> PKC> IRS-1 Phosphorylation on ser
  3. insulin receptor pathway changed
115
Q

adipokines

(released by adipocytes)

A

adiponectin (anti-hyperglycaemic)
activate AMPK/IRS1/2
^insulin sensitivity/ glucose uptake

116
Q

AMPK

A

enzyme promoting liver lypolysis

117
Q

PPAR gamma

A

nuclear receptor > adipocyte differentiation
^secretion of anti-hyperglycaemic adipokines

in liver/ muscle

118
Q

inflammation

via adipocytes

A

adipocytes> IL-6/IL-1

attracts macrophages to fat deposits

119
Q

diabetes T2 therapy

A

diet/ exercise to prevent
medication (thiazolidinediones/ metformin/ sulphonylureas)
insulin (when fully developed)
selective beta 3 agonists
alpha 2 adrenoreceptor antagonists
GLP-1 receptor antagonists
SGLT-2 inhibitors

120
Q

thiazolidinediones

A

PPAR gamma agonist
^expression/ secretion of anti-hyperglycaemic adipokines
sensitizing cells

^lipolysis

121
Q

metformin

A

decreases glucose liver release
AMPK activation
^liver lipolysis/insulin receptor signalling

122
Q

sulphonylureas

A

bind to sulphonylurea receptors on beta membranes
block K+ beta channels depolarize
Ca2+ open / allow insulin secretion via exo

123
Q

selective beta 3 agonists

A

b 3 adrenoreceptors control fat cell lipolysis

124
Q

alpha 2 adrenoreceptor antagonists

A

^insulin secretion

125
Q

GLP-1 receptor agonists

glucagon-like peptide

A

^insulin secretion from beta
pro-survival effect on beta
renoprotective

126
Q

SGLT-2 inhibitors

A

^glu excretion in urine
^ketogenesis

127
Q

long term T2 Diabetes complications

A

macrovascular disease (med/l bv damage)
microvascular disease (small bv damage)

caused by ROS/AGEs generation

128
Q

macrovascular disease results

A

coronary artery disease
cerebrovascular disease
peripheral vascular disease

129
Q

microvascular disease results

A

retinopathy
nephropathy
neuropathy

130
Q

ROS generation

A

generated by FFA/ glucose increase
>micro/macrovascular complications

131
Q

AGEs generation

A

AGE cross-linking to proteins/ receptor binding (RAGE/ AGE-R1)

RAGE> ROS generation/inflam/metab defect

AGE-R1> AGE clearance and ROS decrease

132
Q

AGE collagen cross-linking lead to vessel damage

A

endothelium basal membrane thickening/ LDL trap/ IgG
inflam/ complement/oxidation

133
Q

NFkappaB pathway sequence

effector, signalling pathway and response

A
  1. TNF receptor
  2. IkappaB kinase comple
  3. NF kappa B txn factors
134
Q

what activates NF-kappa B complex

A

DNA damage
infection
hypoxia
physical stress

environmental challenges

135
Q

responses to NF kappa B pathway

A

repair
gene expression
programmed death
immune response

136
Q

2 types of NF-kappa-B signalling pathways

A

canonical
non-canonical

137
Q

canonical NF kappa beta pathway

e.g?

A
  1. TNF receptor stimulated
  2. IKK complex activated
  3. p50/p65 enter nucleus and ^ txn of target genes

e.g. inflam programme

138
Q

IKK Complex activation

in canonical

A
  1. beta phosphorylates IkBalpha inhibitor
    (p50/65 kept in cytoplasm)
  2. IkBalpha proteasome targetted

Complex = IKK alpha beta gamma

139
Q

IKK complex

A

alpha / beta > catalytic activity
gamma> regulatory

140
Q

non-canonical NFkappaB pathway

LTbetaR example

A
  1. NIK kinase phosphorylates IKK alpha
  2. IKK alpha phosphorylates p100> p52 (NFkB active dimer)
141
Q

RHD

Rel homology domain

A

encodes DNA binding/ dimerisation functions of NFkB

142
Q

P100/105

A
  • proteolytically processed to p50/52
  • ankyrin repeats in C-terminal
  • (function as IkappaB inhibitors!!@!!!!)
143
Q

non-conserved txn activation domains

A

TA1/TA2/ TAD/SD1/SDII

144
Q

Cancer associated inducers of aberrant NF-kappa B activity

A

cytokines/ injection/ microflora
oncogene activation
carcinogens/ tumour promoters
stress RO1 inducers
genetic alteration
carcinogen/ tumour promoters
cancer therapies

145
Q

tumor promoting functions of aberrant NFkB activity

A

inflammation
angiogenesis
metastasis
survival
proliferation
immortality

tumours expressing aberrantly active NFkB have altered NF-kB proteins

normal = cytoplasmic and controlled
disease= uncontrolled and nuclear

146
Q

p53 structure

A

N-terminal domain (trans act./ proline rich)
core domain (seq spec DNA binding)
C-terminal domain (tetramerization/ reg non spec DNA binding)

147
Q

P53 inducers

A

hypoxia
nutrient deficiency
oncogenic signalling
oxidative stress
hormones
physio processes

148
Q

P53 inactivator

A

HDM2

degraded when proteasome degrades

149
Q

results of p53-casued cell cycle arrest

A

DNA repair
metabolic switch
cell differentiation
senescence
programmed cell death

programmed cell death > apoptosis/ necrosis/ ferroptosis/ necroptosis

150
Q

cross-talk

between non-canonical NFkB and P53 pathways

A

p53 can inhibit p52 target genes
p52 can repress some p53 target genes/ co-regulate p53 target genes

151
Q

NFkB in cancer cells

A
  • can become tumor promoter
  • loss of tumor suppressor/ reg genes> aberranty activation
152
Q

senescence regulation

regarding cross-talk between non-canonical NFkB and p53

A

p53 activates p21
p52/RelB/BCl3 ass. senescence p53 dependent

induces senescence growth arrest
blocks pRB E2F pathway for cell prolife

153
Q

EZH2

A

expression induced upon CD40L stimulation of primary B cell lymphocytic Leukaemia cells

can work as oncogene

BMS2002 (5 decks)

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