LMD Lecture Flashcards

1
Q

six steps of cell-cell communications

A

synthesis, release, transport, detection, change, removal

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2
Q

Large distance extracellular signalling is mediated by

A

hormones

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3
Q

Short distance extracellular signalling is mediated by

A

neurotransmitters and some growth factors

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4
Q

Autocrine signalling mediated by

A

growth factors

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5
Q

Autocrine signalling generally act on themselves to ____

A

regulate proliferation

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6
Q

Growth factors have which modes of communication?

A

All three

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7
Q

Epinephrine have which modes of communication?

A

Endocrine and Paracrine

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8
Q

4 types of intracellular signalling

A

Contact dependent, paracrine, synaptic, endocrine

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9
Q

3 types of signalling according to distance

A

endocrine, paracrine, autocrine

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10
Q

How was cell communication discovered?

A

Protrusion of yeast cells

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11
Q

Difference between synaptic and endocrine

A

(1) One neurotransmitter - many actions, hormones require specificity, (2) endocrine - bloodstream, synaptic - neural transmission, (3) endocrine - operates over a longer period of time, synaptic - immediate response to signal
- the endocrine system secretes hormones into the bloodstream and the nervous system secretes neurotransmitters which are released directly onto their target cells.
- the nervous system responds faster than the endocrine system.
- the nervous system typically activates its targets quickly and only for as long as action potentials are sent to the target. The endocrine system tends to have longer-lasting effects.

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12
Q

Lipid soluble hormones

A

Steroids, thyroid hormones, retinoids

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13
Q

Steroids are from

A

lipids derived from cholesterol in SER

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14
Q

What provides uniqueness for steroids

A

different fxnal groups around core structure

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15
Q

Steroids turn on what…

A

GENES!

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16
Q

Function of thyroid hormones

A

help set basal metbaolic rate, activate enzymes involved in catabolism of fats and glucose

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17
Q

Vitamin A derivatives and their functions

A

Retinoids, effects on proliferation & differentiation plus cellular death

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18
Q

Water soluble hormones

A

amino acid derivatives and eicosanoids

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19
Q

Modified AA hormones

A

serotonin, melatonin, histamine, epinephrine

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20
Q

Large peptide hormones

A

insulin and glucagon

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21
Q

Eicosanoids are derived from

A

arachidonic acid

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22
Q

Examples of eicosanoids

A

prostaglandins and leukotrienes

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23
Q

Action of prostaglandins

A

ACT ON CELL SURFACE RECEPTORS DESPITE BEING LIPOPHILIC

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24
Q

How do water soluble hormones act?

A

Bind to cell surface receptors –> second messenger system

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25
Q

Narrate mechanism of vessel dilation

A

Neuron secretes neurotransmitter, Ach binds to Ach receptor in endothelial cell producing NO which increases GMP leading to vessel dilation

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26
Q

NO’s mode of cell communication

A

PARACRINE

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27
Q

T/F. NO is stable.

A

F

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28
Q

T/F. NO has local effects and is NOT systemic

A

T

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29
Q

8 examples of neurotransmitters

A

Acetylcholine, glycine, glutamate, GABA, dopamine, serotonin, epienephrine, histamine

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30
Q

How do neurotransmitters work/

A

They bind on cell surface receptors that induce conformation chane on ion channels causing ion influx

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31
Q

Activators of NMDA receptor

A

Glycine glutamate

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32
Q

Antagonist of NMDA receptor

A

Homocysteine, TCF

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33
Q

3 classes of cell surface receptors

A

GPCR, ion channel, enzyme coupled

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34
Q

Examples of GPCR

A

epinephrine, glucagon, serotonin

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35
Q

GPCR is involved in

A

light detection (eye), odorant detection (nose), detection of certain hormones and neurotransmitters

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36
Q

Two types of G proteins

A

Gs and Gi (stimulates, inhibits)

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37
Q

Example of ion channel receptor

A

Ach receptor

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38
Q

Where are ion channel receptors

A

Neuronal plasma membrane, plasma membrane of muscle cells

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39
Q

Functions of ion channel

A

saltatory conduction, muscle contraction

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40
Q

Cytokines and interferons are what type of receptors

A

Tyrosine kinase linked receptors

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41
Q

Examples of non catalytic receptors that are coupled to tyrosine kinases

A

Erythropoietin, inteferon

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42
Q

Binding of a ligand on Tyr kinase-linked receptor results into

A

Dimer formation then activation of tyrosine kinases

43
Q

Difference between RTKS and Tyr kinase linked receptors

A

RTKs have intrinsic catalytica ctivity

44
Q

What binds to RTKs

A

Growth factors - peptide/protein hormones such as NGF, PDGF, insulin

45
Q

What AA residues are phosphorylated by RTKs?

A

serine, threonine

46
Q

A and B must be present to activate Y., What’s Y?

A

Integrator protein

47
Q

Another name for Y if A and B must be present to activate Y

A

Coincidence detector

48
Q

Enhances speed, efficiency and specificity of response

A

Scaffold protein

49
Q

Site at which GTP binds on G protein

A

ALPHA SUBUNIT

50
Q

What is activated by Gs alpha subunit

A

Adenylyl cyclase

51
Q

Second messengers

A

cAMP, IP3, DAG, Calcium

52
Q

What receptor of a signal pathway is not being participated by cAMP

A

RTK

53
Q

function of cAMP

A

activate PKA

54
Q

Regulates cAMP to shut off the signal

A

phosphodiesterase. pyrophosphate becomes driver for cAMP synthesis

55
Q

Effects of PKA activation

A

on adipocytes: stimualte production of FA, on ovarian cells: increase estrogen

56
Q

PKA phosphorylates glycogen phosphorylase causing activation. T/F

A

True

57
Q

PKA phosphorylates glycogen synthase causing activation. T/F.

A

False

58
Q

Low cAMP levels trigger GPCR to produce PKA.

A

False. Epinephrine triggers GPCR increasing cAMP, and PKA in the process. Epinephrine is a stress hormone and the activation of PKA leads to glucose utilization activating glycogen phosphorylase and inhibiting glycogen synthase.

59
Q

GPCR acts to 2 enzymes relevant in our discussions

A

adenylyl cyclase and phospholipase C-Beta

60
Q

GPCR A subunit —> ??? —> ____ + _____ –> Calcium release

A

??? is phopholipase C B, IP3 and DAG

61
Q

DAG acts on

A

Protein Kinase C

62
Q

IP3 acts on

A

ER to release calcium

63
Q

Effects of calcium

A

Exocytosis of insulin, muscle contraction, Ca-calmodulin affecting gene expression

64
Q

MAP kinase pathways are activated by

A

RTKs

65
Q

MAP kinase pathway: ___ –> ____ —> MAP Kinases

A

Ras GTPase —> rac —> MAP kinase

66
Q

MAPK activation leads

A

translocation into nucleus and phosphorylate proteins

67
Q

Central driver of MAP kinase paths

A

cdc42/rac

68
Q

Stress reponse and apoptosis

A

rac-MEKKs-MEK 3/6-p38MAPK->MAPKAP2 or ATF and elk. MAPKAP2 leads to hsp27

69
Q

Stress response and proliferation

A

rac-MEKKs-JNKK1/2-JNK1/2-ATF,jun,elk

70
Q

Proliferation and differentiation

A

rac-ras-raf-MEK-ERK-elk,RSK,fos

71
Q

Complete: ras-__-___-___-___ or _____

A

ras-raf/MAPKKK-mek/MAPKK-erk/MAPK–change in protein activity or change in gene expression

72
Q

Negative regulator of water soluble hormones

A

phosphodiesterase

73
Q

Parts of a nuclear receptor

A

transcription activating domain, ligand binding domain, DNA binding domain

74
Q

Inhibitory proteins bind to the C-terminal portion of an inactive protein in the nuclear receptor superfamily. T/F

A

T

75
Q

Nuclear hormone receptor binds to DNA has heterodimers. T/F.

A

F either hetero or homo

76
Q

What stabilizes ligand in a nuclear receptor protein?

A

Alpha helix in C terminal portion.

77
Q

Binds to transcription activating domain to allow DNA binding element to bind successfully.

A

Coactivator proteins

78
Q

___ activates ___ leading to ___. Example is estrogen.

A

Steroids or the nuclear receptor superfamily of proteins activate early primary response genes leading to activation of delayed secondary response genes.

79
Q

Narrate gene activation pathway

A

1o transduction - relay - transduce and amplify - integrate - spread - anchor - modulate - effector protein activation

80
Q

Cell death receptors belong to ___ family

A

TNF family

81
Q

Classic cell death receptor

A

Fas

82
Q

Ultimate effectors of apoptosis and the reason for their name

A

Caspases. Have Cys in active site and cleave after Asp

83
Q

Regulators of apoptosis

A

Bcl2 family

84
Q

Intrinsic pathway of apoptosis

A

Mitoc damage - cytochrome C release - caspase activation

85
Q

B1 integrin activates

A

MAPK cascade

86
Q

Classes of CAMS

A

cadherins, Ig like superfamily of CAMs, integrins

87
Q

cell-cell adhesion

A

ig like superfamily of CAMS, cadherins

88
Q

calcium dependent

A

cadherins, integrins

89
Q

ca independent

A

Ig superfamily

90
Q

homophilic, binds to same CAMS

A

ig superfamily of CAMS and cadherins

91
Q

heterophilic

A

ig superfamily of CAMS and integrins

92
Q

junctions containing cadherins

A

adherens junction, desmosome

93
Q

has cadherin, ties actin together

A

adherens junction

94
Q

has cadherin, ties actin together

A

desmosome

95
Q

ECM with cytoskeleton

A

integrins

96
Q

Integrins mediate cell-cell interactions. T/F.

A

T weakly nga lang

97
Q

number of integrin alpha and beta subunits

A

17 and 8

98
Q

three components of ECM and their functions

A

collagens - structural framework for strength and resilency, proteglycans – cushions cells, adhesive matrix proteins - binds these components to receptors on cell surface

99
Q

Junctions of integrins, identify connected molecules

A

focal adhesions (FN to actin), hemidesmosomes (IF to collagens & laminins)

100
Q

Integrins trigger cell signalling through…

A

focal adhesion kinases

101
Q

____ make up ___ to allow free passage of ions from cell-cell

A

connexons make up gap junctions

102
Q

two molecules allowed to traverse through gap junctions

A

Ca and CAMP

103
Q

What does NO bind to?

A

Guanylyl Cyclase (converts GTP to cGMP)