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Cell communication Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is contact dependent signalling?

A

membrane bound signal molecule attaches onto target cell

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2
Q

What is paracrine signalling?

A

signalling cell produces local mediators that affect surrounding target cells

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3
Q

What is endocrine signalling?

A

endocrine cell produces hormone that is widely acting and circulate through the body to impact target organs

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4
Q

What is a morphogen gradient?

A

responses occur at specific thresholds instead of qualitatively, there are uncommitted or committed cells

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5
Q

Positive feedback

A

short stimulus causes fast response becauase the products positively regulate each other so the system maxes out and is sustained beyond stimulus

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6
Q

Negative feedback

A

stimulus causes response which maxes out but then goes away when the stimulus does as one product is negatively regulating the other

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7
Q

How do kinases work?

A

control signalling by phsophorylation and work by inhibiting ATP binding pockets so it can’t bind, preventing a response

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8
Q

What are the three essential functions of ion channels?

A

transport of ions across membrane
regulation of membrane potentials in nerve and muscle cells
influx of Ca2+ into cytoplasm for contraction/secretion

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9
Q

Common ion channel structure

A

transmembrane domains usually made of 2 or more alpha helices
2-6 subunits that surround the pore

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10
Q

What is a simple K+ ion channel made up of?

A

TM helicase structures that form a p-loop that is highly selective as the cytoplasmic side TMs are more tightly packed- selectivity filter
S1-4 TMs, S5+6 form p-loop

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11
Q

What are factors that can control a simple K+ channel?

A

membrane potential
mechanical stress
ligands

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12
Q

What are the two main functions of voltage gated ion channels?

A

to create action potentials in excitable cells
transport Ca2+ into the cytoplasm as a 2nd messenger

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13
Q

What is different about voltage gated channels struture compared to simple ones?

A

additional helices S1 and S4 form a seperate voltage sensing domain lateral to subunits
large polypeptides that extend into cytoplasm
plugging mechanism

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14
Q

What are transient receptor potential channels?

A

share common structural features with voltage gated but evolved to sense chemicals and stimuli

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15
Q

Ligand gated channels

A

similar to voltage gated but are controlled by the binding of a ligand, either intracellular or extracellular
3 out of 4 subunits must be bound to induce response

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16
Q

What types of channels have cytoplasmic anchors?

A

voltage gated
TRP
ligand gated

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17
Q

Cys-loop type receptors

A

pentametric

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18
Q

nAChrs

A

cys loop
5 subunits with 4 TMs each
chronic exposure leads to receptor upregulation
in muscle

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19
Q

What do mutations in nAChrs cause?

A

M2 region of human a4 neuronal subunit mutated
autosomal dominant nocturnal frontal lobe epilepsy due to receptors having delayed repsonse to NTs, causing a lag and no recycling of NTs which increases their concentration

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20
Q

Types of glutamate receptors

A

Kainate
NMDA
AMPA

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21
Q

What are NMDA receptors important for?

A

controlling synaptic plasticity
mediating learning and memory

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22
Q

Glutamate receptors

A

trimeric, similar structure to ACh but pore is inverted and binding site is a cleft that closes when occupied
vital to every aspect of brain function

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23
Q

P2X receptors

A

trimeric and are ATP gated ion channels
3 subunits and 2 TM helices with a large extracellular domain
3 ATP molecules needed to open channel

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24
Q

General structural features of GPCRs

A

7 transmembrane domains which are all alpha helices
TM 3- centrally located next to binding pocket
extracellular N terminus for ligand binding
intracellular C terminus for G protein binding

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25
Q

G proteins

A

guanine nucleotide binding proteins
belong to the GTPase family
heterotrimeric- alpha, beta and gamma domains

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26
Q

How do G proteins act as molecular switches?

A

hydrolyse GTP to GDP
GTP- on
GDP- off

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27
Q

How are GPCR classes distinguished?

A

structural features of the extracellular domains defining the ligand binding site
linked directly to the diversity of stimuli GPCRs can detect

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28
Q

Protease activated receptors

A

proteases activate receptors in platelets by cleavage of the N terminal, which acts as a tethered ligand
part of the receptor itself acts as an agonist
platelet activation by- thrombin, ADP + basal lamina

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29
Q

How are GPCRs turned on?

A

inactive state is when GDP is bound to alpha subunit
ligand binds causing conformational change that activates G protein
GDP released and alpha subunit seperates from beta/gamma to bind GTP
now is active and binds to target protein in membrane to elicit response

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30
Q

How do G proteins act as timers?

A

the duration of signalling activated by G proteins is regulated by the rate of GDP hydrolysis by the alpha subunit
RGS proteins stimulate GTPase activity in alpha subunit

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31
Q

How many families of G proteins exist?

A

6

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32
Q

GPCRs compared to ion channels

A

they are slow to open or close
but stay open/closed for longer

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33
Q

How can active G proteins regulate the activities of enzymes that control 2nd messengers?

A

small molecules carrying signals to hydrophobic lipids confined to the membrane
small soluble molecules that diffuse throught the cytoplasm like cAMP and cGMP
calcium

34
Q

How are mutations in GPCRs linked to cancer?

A

90% of uveal melanomas have mutations in Gq alpha subunits
leads to blocking of GTP hydrolysis so subunits are always active- permanent signal transduction of growth pathways

35
Q

Adenylate cyclase

A

has 10 isoforms and is a membrane anchored enzyme
activated by Gs alpha subunit
inhibited by Gi alpha subunit

36
Q

Gs mechanism

A

ligand bind to receptor activating g protein
alpha subunit moves and binds to adenylate cyclase in the membrane
activated adenylate cyclase catalyses formation of cAMP from ATP
cAMP activates PKA which then phosphorylates and activated protein to initiate response in cell

37
Q

How is Gs signalling switched off?

A

agonist dissociating from receptor
GTPase activity on Gs
cAMP broken down by phosphodiesterase
dephosphorylation of enzymes

38
Q

cGMP second messenger system

A

similar to cAMP except enzyme is guanylate cyclase which is receptor bound or free in cytoplasm
converts GTP to 3’-5’ cyclic guanosine monophosphate

39
Q

What is the local concentration of 2nd messengers determined by?

A

rate of production
rate of diffusion from site of production
rate of removal

40
Q

What molecules regulate concentrations of cAMP?

A

production is regulated by adenylyl cyclase
removal is by phosphodiesterase

41
Q

What 2 types of messengers can be generated by phospholipase C?

A

IP3- water soluble and diffuse through the cytoplasm
DAG- hydrophobic molecules that remain in the membrane

42
Q

Where does specificity in signalling come from?

A

selective expression and cellular localisation of signalling molecules

43
Q

Protein Kinase Cs

A

Ser/Thr kinases that are activated by DAG and Ca2+

44
Q

PMA phorbol ester

A

an analogue of DAG used in research to activate PKCs

45
Q

DAG binding mechanism

A

causes dissociation of intramolecular psuedosubstrate domain from the active site
once activated PKCs provide either positive or negative feedback in pathway

46
Q

Phosphorylation of phospholipase C

A

provides negative feedback for GPCR signalling and makes it transient

47
Q

What cellular functions does calcium regulate?

A

synaptic transmission
hormone secretion/synthesis
fertilisation
muscle contraction
cytokinesis

48
Q

Cytosolic Ca2+ in resting cells

A

kept low at 100nM by ATP driven Ca2+ pumps
this is important for its job as a 2nd messenger

49
Q

How is Ca2+ concentration regulated?

A

influx regulated by channels in the extracellular membrane and ligand gated ion channels on ER

50
Q

How are ER calcium and store levels refilled/maintained?

A

store operated channels made up of ORAI and gated by STIM

51
Q

What does overstimulation of GPCRs lead to?

A

tachyphylaxis (LSD or salbutamol)
disease such as uncontrolled growth in cancer

52
Q

How is overstimulation of GPCRs prevented?

A

GRK (receptor kinases)
B-arrestin
stops G protein from binding and internalises receptor so its degraded or recycled

53
Q

What channels are an exception to the standard 2-6 subunits that surround the pore usually?

A

chloride, water and ammonia channels
exist in the middle of a single subunit

54
Q

What are ion channels classified into subgroups based on?

A

gating mechanism (voltage or ligand)
ion seletivity of the pore, defined by the physical size of the filter and the amino acids that line it

55
Q

Alpha helices

A

right hand helix conformation

56
Q

Beta sheets

A

beta strands connected laterally by at least 2 or 3 backbone hydrogen bonds forming a sheet

57
Q

Subunit

A

single protein that joins with others to form protein complex

58
Q

Transmembrane domain

A

protein that spans the width of the membrane form the extracellular to intracellular sides usually with a helical shape

59
Q

P loop or pore

A

pocket where an ion will bind

60
Q

What types of channels have plugging mechanisms?

A

voltage gated
TRP

61
Q

Na+/K+ selective channels

A

control membrane excitability and depolarise cells

62
Q

Ca2+ channels

A

directly regulate the activity of calcium sensitive proteins

63
Q

Cl- selective channel

A

control membrane excitability by reducing resistance and hyperpolarising cells to reduce AP firing

64
Q

a4b2

A

neuronal nAChRs abundantly expressed in the cortex and hippocampus
have a high affinity to agonists nicotine and varenicline

65
Q

What is linked to tobacco dependance but better cessation outcomes?

A

CHRNA4 (a4)
CHRNA6 (a6)

66
Q

AMPA

A

mediate fast excitatory synaptic transmission in the CNS

67
Q

NMDA

A

involved in learning and memory and is slower than other isoforms

68
Q

Kainate

A

similar to AMPA but lesser role at synapses
linked to schizophrenia, depression and huntingtons

69
Q

RNA splicing in AMPA

A

each subunit exists as 2 splicing isoforms flip + flop

70
Q

What does alternative splicing of 2 exons in the primary transcript lead to? (AMPA)

A

2 protein isoforms with different domains in the extracellular loop that have different kinetic properties

71
Q

What are the different kinetic properties of flip and flop?

A

flop has a faster desensitisation rate and reduced current responses to glutamate than flip

72
Q

What is the effect of a lack of GluA2 RNA editing?

A

mutant mice lacming enzyme responsible for RNA editing prone to seizures and early death

73
Q

GluA2 Q/R site

A

located in the M2 of subunit inside the channel pore
Glu codon to a Arg codon

74
Q

Downregulation of GluA2 Q/R editing in motor neurons of ALS patients leads to…

A

increase in Ca2+ permeable AMPA receptors
causes damage due to glutamate excitotoxicity

75
Q

What is decreased ADAR activity linked to?

A

increased malignancy in glioblastoma
increase in Ca2+ means Akt pathway promoting proliferation/tumourigenesis is increased
reversed when GluA2 Q/R was edited- potential target

76
Q

Diseases/physiological conditions linked to PX2/trimeric receptors

A

P2X2 hearing loss
P2X4 pain
P2X7 inflammation + neurodegenerative disease

77
Q

Diseases/physiological conditions linked to glutamate/tetrameric receptors

A

excess NMDA in stroke = neuron death

78
Q

Disease linked to cys loop receptors

A

epilepsy

79
Q

Lipid kinases

A

add phosphate groups to lipids

80
Q

What do loss of function mutations in Orai1 cause?

A

have an important role in activation of t lymphocytes so causes severe combined immunodeficiency

Molecular and cell biology (8 decks)

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