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UE2 Biocell > Apoptose-differenciation > Flashcards

Apoptose-differenciation Flashcards

1
Q

la sencescene est due in vitro au nb limite de diviosns mitotiques

A

oui

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2
Q

la seq telomerique se raacourcit a chaque divioan ussi in vivo que in vitro

A

yes

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3
Q

immortalite peut etre due a une abs de la prot p53

A

oui

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4
Q

immortliete peut etre due a p21 inactif

A

oui

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5
Q

qui est un suicide cell

A

apoptose

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6
Q

autophagie conduit tjs a la mort

A

non survie parfois

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7
Q

apoptose controle que par des facteurs exogenes

A

non aussi endogenes

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8
Q

apop: permet de creere et de detruie des struc

A

oui

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9
Q

cancers : apoptose role majeur

A

yes–> moins apoptose

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10
Q

appoptose controle le nb de cell

A

yes

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11
Q

nom de necrose du muscle cardique

A

infacrtus du coeur

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12
Q

il existe une necrose physio

A

non

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13
Q

elle se dsitingue POINT par POINT de l’apopotose

A

yes

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14
Q

origine de la necrose

A

belssure donc path

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15
Q

3 etapes reversibles de la necrose

A
  1. gonflement des organites 2. formaitojnde struc myelin like 3. deformation dela MP (bulles)
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16
Q

necrose se progage ct

A

explosion MP ==> lib enz lyso ==> damage nearbuy cells

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17
Q

necrose associe a la cicatrication

A

oui anacrhcique par les fibroblatses = fibroses

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18
Q

qiu augmente atuphagie

A

carence en nurtiments en carence en E

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19
Q

membrane IC d’isolation : simple membrane

A

non double m

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20
Q

4 stades d’une cell en autophagie

A
  1. double m disolation 2. phagophore (elongation + cargo) 3. Autophagosome (fermeture) 4. autlysomes (fusion ac lysosomes)
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21
Q

a q stade fermeture de la m en autophagie

A

autaphagosome

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22
Q

autophagosome = stade final

A

non autolysosome

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23
Q

autophagie apicale courante

A

non quasi toutes les cell ont une autophagie BASALE

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24
Q

role physio de autophagie

A

DDILNH (dvt diff immunite logtivite nutrition homeostaie

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25
Q

qui DDILNH (dvt diff immunite logtivite nutrition homeostaie

A

autophagie

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26
Q

trop ou pas assez autophagie si inflammation chronique

A

trop

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27
Q

trop ou pas assez autophagie si diabete et obseite

A

trop

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28
Q

trop ou pas assez autophagie si maladies infectieuses

A

pas assez

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29
Q

trop ou pas assez autophagie si cancer

A

les 2

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30
Q

consequences si torp autophaguie

A

diabete/obesite - cancer - neurodegen - inflammation chroni - maladies hepatiques - maladies cariues et vascu

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31
Q

maladie hepatiue : trop ou pas assez autophagie si

A

torp

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32
Q

impact if too few autophagie

A

patholiges infectieuse set cancer

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33
Q

4 destins cell

A

cycle cell - apotose - sencescn - differenctiation

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34
Q

il y a une voie apoptose

A

non 2 : intrinsqie (si pbs ADN) et extrin (receptuers de la mort)

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35
Q

2 voies de apotpose interconnecte

A

yes

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36
Q

caspase extrin 8 ou 9

A

8

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37
Q

caspase mito

A

9

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38
Q

casp 3 activee par qui 5/5

A

caspase 9 et 8

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39
Q

nature des caspase :

A

cysteine proteases

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40
Q

caspase clivent q prot

A

prot ac cysteine

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41
Q

m struc casp effectrice et initatrice

A

non prodomaine splus longs pour nitiatrice

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42
Q

qui est le substratd des caspases initritrices

A

les caspases effectrices

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43
Q

qui controle act des caspases

A

domaine de liaison sur leur prodomaine

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44
Q

procaspase initriatrices s’autoclivent

A

yes

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45
Q

caspase ont de multiples subst

A

YES

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46
Q

caps affectes presque toutes les fonctions cell

A

yes

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47
Q

substartas des casp

A

prot truc - signalisation - metabo ADN/ARN - facteur nucelaire et du cycle cell

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48
Q

TOUTES les consequences du clivage des subtra par les casp conduit a apotose

A

yes

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49
Q

substart des caspase prot struc

A

gelsoline lamines actine keratines fodrine

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50
Q

substart des caspase prot de signalisiation

A

pls kinases

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51
Q

substart des caspase prot ‘facteur nucelaire’ et prot du cycle cell

A

rb et cycline A2

52
Q

clivage par les casp induit que perte de fonciton

A

non aussi gain de fonctin (clivage debid –> act de la voie intrinseque = clivage des caspases –> activaiton de apotose

53
Q

pq inactivation de la polymerisationa a-ctine

A

clivage de gelsoline

54
Q

=> clivage des lamines

A

destabi env nuc et fragmentation du noyau

55
Q

substart des caspase prot du metabo adn arn

A

ply adp ribose polymerase
dna dpdt protein kinase
histone H1
hnRNPC - ribonucleoprot

56
Q

ct suicide cell

A

condensation adn (casp cliventH1 et dna dpt kinases) - fragmentation de noyau (lamines - actine - gelsoline clivee)

57
Q

qui controle initiaion et deroulement de l’apoptose

A

p53

58
Q

formation de apoptosome dpd de qui

A

lib du cytochrome c par mitochondrie

59
Q

qd p53 recrute

A

si pb adn

60
Q

apoptosome voie intrinsque ou extrin

A

intrin

61
Q

elements de l’apoptosoome

A

APAF1 - casp 9 - cytp C qui permet assenmlabe

62
Q

ct caspase 9 active

A

apotomse formee -> autoclivaiton decasp 9 possi

63
Q

qui controle lib du cytochrome c

A

famille de prot bcl2

64
Q

prot bcl2 un grupe

A

non 2 : pro apot vs antiapoto

65
Q

struc des bcl2

A

bcl homology domains = BH -> domaine transmem - bcp helices => compact ==> peut interagir avec d’auyres familles

66
Q

quelles prot de la famile bcl2 controlent staut apoti

A

monomeres : bcl2 (antiapop) - bax (proapoto)

cs bcl-xL/bim

67
Q

xs de prot bcl que effet proapop

A

non certains cx anti apop et d’autres pro apop

68
Q

meca apoptose big pic

A

apop –> fragmenttio noyau –> capsane clivent des subtrats –> casp voie intr activvee par cytochrome c –> lib cytichrome c controlle par es prot bcl2

69
Q

prot de regulation fine de la voie intrinseque

A

bcl2 - bid - smacdiablo - IAPs p53

70
Q

ds cancer qui cibler

A

bcl2 - bid - smacdiablo - IAPs p53 = prot regu de apotose pour restaurer apoptose

71
Q

caract des cancers controles par p53

A

dommages a ADN, proli anormalae, erosion des teomeres, hypoxie angiogenene, invasion metastastqie, chimioresistqne

72
Q

struc de p53 necessaire pour sa fonction

A

domaine fonctionnel specialise ds reconnaisande de adn ds lequel adn endommage peut se fixer –> p53 synthei des facteurs de trascn qui orienta act trans –> apoptose ou progrssion ds cycle si adn repare

73
Q

voie extrin: fixation du ligand induit dimerisaion du recepteur

A

non trimerisation

74
Q

apaf1 = prot adaptirece de voie extr

A

non c’est FADD

75
Q

recepertue a DED

A

non DD c’est adaptai et casp iniqui a DED

76
Q

ele de DISC

A

ligand - receptue (trimerise) - fadd - casp8

77
Q

qui initie voie extrin

A

ACTivation des recepteurs de sigaux de mort

78
Q

senescen synonyme de quiescence

A

non

79
Q

sensecen arret reversible du cyccle cell *****

A

non IRRE m si facetur oncogenes ou mitorgenes

80
Q

quel phenomene dus aux stress

A

sences

81
Q

senes: peut avoir un contrnu adn a 4n

A

ou

82
Q

m activite metabo pour cell senceet quiescente

A

non sencesnece act metabo +++

83
Q

cause sence patho

A

stress oxydant RE meta - dommage a ADN - oncogene

84
Q

oncognes causes sence patho

A

yes

85
Q

maruquers d;une cell secne : telomeres courts

A

yes

86
Q

cell somatique normale ADN elomerase lit adn juqua bout

A

non telomerease

87
Q

telomere se raccourcit de cb de n par mitose (**)

A

50-200

88
Q

taille telomere

A

5-15 k bases

89
Q

cell germinale t somatique ont la m qte de telomerase

A

non germinale : telo++++

90
Q

limite de hayflick

A

nb de mitoses

91
Q

q prot rajoute des telomeres

A

hTERT

92
Q

les faceurs de stress peuvent induire une senece prematuree

A

yes

93
Q

fac de streess crrent tous des dommages sur A

dn

A

yes

94
Q

culture cell est un fac de stress

A

yes

95
Q

6 causes de sence et dc de dommage a ADN

A

culure cell - activation des telomeres -
medocs cytotox -
stress metabo et ocydantanomalie des telo -

96
Q

celll osteoprognitrices ou souches ont pus de telomerseq

A

cell osteoprg

97
Q

relation entre sence et apotoseq

A

art of the DDR (dna damage response)

98
Q

DDR def

A

dna dammagrespon = voie de reponse par signalisarion et mecanisme mol enzym

99
Q

sene: faible act metabi

A

non ACTIVE

100
Q

que secretne secen

A

IL chemokines receptuers et ligands facteurs de crossamce (EGF eg) proteases (eg MMPs)des fac nisolubles(collagne)

101
Q

action des cell sence

A

SASP autocrine ou paracrine

102
Q

esperance de vie hommet celle de vie en bonne sante

A

79 ans et 63an

103
Q

esperance de vie femme celle de vie en bonne sante

A

85 ans- 65

104
Q

vieillist est une malade

A

non mais ac le vieill les maldaes + frequent

105
Q

on viellit en fonciton du patrimoine de envi et des stress subies

A

ues

106
Q

maladies liees a la sence frequentes

A

rare

107
Q

2 maladies DIRECT liees a la sence

A

progeria –> mutation gene lamine A

Werner : mutation du gene WRN de helicase

108
Q

maladies aaso a la sec rare

A

non fre : osteoporose athroscle alzeimer cancer

109
Q

progeria et syndorme de erner = asso a ala sence

A

non directement liees

110
Q

marqueurs de la sece

A

DDR et perte de lamine B1

111
Q

2 devenir des cell secn

A

cancer ou veilli

112
Q

ct netoyage des cell secn

A

cel immu grace au sasp ==> regression tumorale suppresion tumorle homeostaie tissulaire dvt embyrommare rajeunissenemtn regeneratipm

113
Q

diff: arrte du cycle irrev

A

non reversible mais durab;e

114
Q

q stades cell totitpotentes

A

blastocytes

115
Q

def cell totipotenet

A

cell qui peut se diff e tout

116
Q

celll totipotentes oeuvent donner naidsance a quoi

A

cell unipotentes ou mutiliporen

117
Q

organogene a besoi n de cell totipotenes

A

yes

118
Q

def diff

A

selection d’un panel de gene

119
Q

genes de la proli exprimees partout

A

non pas chex les cell diff

120
Q

perturbation de diff peutmeener au cncer

A

yes

121
Q

IPS = reprogrammation cell

A

yes

122
Q

def ips

A

redonner des carct de cell totipotenes a des cell diff g a 4 genes : oct3/4 sox2 cmyc klf4

123
Q

3 facteurs de diff

A

faceuts diffusibles (hormones-fac de trans), MEC (integrines) - contacts cellcell (cadherine_ =fac stochati = hasard

124
Q

caspases : prot nucelaires ?

A

non cytosoliques

125
Q

nom des 3 caspases effecrces (5/5)

A

3,6,7

126
Q

aspect photo d ela necrose (5/5)

A

explosion des organistes ==> boursuflures

127
Q

nuclease clive ADN

A

yes

UE2 Biocell (15 decks)

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