cells final Flashcards

1
Q

HeLa cells immortality

A

overactive telomerase never shortens allowing indefinite replication and division

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2
Q

gene regulation

A

chem modifications to chromatin and histones, during transcription or translation

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3
Q

chromatin

A

dna, rna, proteins packed to give chromosome shape

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4
Q

methylation

A

reversible PTM in nucleus of cytosines occurs in CpG islands near gene promoter and silence transcription, cause gene inactivation
restricts DNA access

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5
Q

histones

A

proteins that provide structural support to chromosomes and bind with DNA to form nucleosome
belong in nucleus
have nuclear localization tag

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6
Q

RNA processing

A

RNA transcript to mRNA by splicing introns, add 3’ polyAtail and 5’ cap. to cytoplasm

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7
Q

srRNA

A

inhibits translation, cause degradation of RNA, silence and inhibit, chromatin remodeling

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8
Q

HAT

A

acetylation makes histones more negative and loosens DNA packing so transcription factors can bind to promoter TATA box

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9
Q

+ control lac operon

A

CAP activation in response to glucose
active/inactive based on glucose - cAMP/CAP levels

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10
Q
  • control lac operon
A

induced or repressed operator
induced by presence of lactose which relieves repressor, promoter recruits RNA polymerase

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11
Q

controls cAMP levels in lac operon

A

rate of bacterial growth

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12
Q

high lactose and high glucose lac operon

A

induced and inactive

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13
Q

negative cell cycle regulators

A

p53, p21, Rb tumor suppressors

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14
Q

positive cell cycle regulators

A

cyclin CDK

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15
Q

EGF binding

A

Upregulating proliferation
Down regulating apoptosis

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16
Q

ZO-1

A

tight junction protein
ZO-1 knockout has increased F actin expression→ actin is a component of microtubules

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17
Q

qRT-PCR

A

dna expression; further left = more transcription/translation

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18
Q

separation experiments

A

TLC, centrifugation, electrophoresis

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19
Q

siRNAs

A

knock down gene in experiments

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20
Q

silencing

A

repress transcription by change gene dosage and rate of transcription

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21
Q

proximate

A

mechanisms

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22
Q

ligand

A

signaling molecule binds to receptor causes activating change

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23
Q

membrane composition

A

TLC by polarity, freeze fracture lipid bilayer, FRAP, pulse chase?

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24
Q

pulse chase

A

trafficking and movement proteins

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25
Q

evolution

A

by natural selection reqs variation that is heritable and results in differential reproductive fitness success

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26
Q

protein destined for ion channel

A

amino-terminal and signal anchor peptide seq

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27
Q

rough ER

A

studded w ribosomes; protein synthesis destined as transmembrane, secreted out, or lumen organelles
default is secretion
COP II move from ER to golgi

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28
Q

lysosomal enzymes

A

vesicles that break down protein; synthesized on rough ER, processed in golgi

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29
Q

Golgi apparatus

A

synthesizes carbs, sorts protein and lipids to final destinations.
PTMs like glycosylation occur here by enzymes
cargo arrives at cis-golgi and exits trans-golgi face
COP I move from golgi to ER

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30
Q

COP I vesicles

A

move golgi to ER

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31
Q

COP II

A

move ER to golgi

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32
Q

ER resident proteins

A

amino terminal sequence

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33
Q

amino terminal sequence

A

ER (lumen) proteins, ion channel protein, secreted
rough ER

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34
Q

Coat proteins

A

make vesicles

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35
Q

destined for mitochondria/chloroplast, ER, secretion

A

amino terminal signal sequence

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36
Q

SRP

A

signal recognition particle is rna-protein complex

37
Q

no signal peptide

A

free ribosome in cytosol

38
Q

Sar I GTPases

A

trafficking
controls coat assembly on coat protein complex II (COPII)-coated vesicles, which mediate protein transport from the endoplasmic reticulum (ER) to the Golgi.

39
Q

GTPases

A

on or off
protein switches regulate cell responses to EC signals
cause cell survival, proliferation
in nucleus to start transcription and gene expression

40
Q

Ras

A

GTPase activates RAF kinase and MEK/MAP growth signal kinase and ERK/MAP
activated by EGFR to cause cell proliferation

41
Q

signaling molecule

A

polar ligand on cell surface like EGF

42
Q

MDM2

A

degrades p53 (- regulator, ubiquinates)

43
Q

p53

A

antagonistically pleitropic bc p21 path allows for apoptosis beneficial early on or stores away and causes aging/senescence
checks for DNA mutations or triggers apoptosis

44
Q

Rb

A

tumor suppressor binds to transcription factors and genes NOT transcribed

45
Q

life history characteristics

A

lifespan
litters/year
reproductive age
maturity
# offspring
parental care

46
Q

(hemi)desmosomes

A

bind to IM filaments and connect w integrins
Integrins and hemidesmosomes bind to ECm basal lamina

47
Q

desmosomes

A

adhesive junction for mechanical stress stability containing cadherins

48
Q

e cadherin

A

uvomorulin
desmosomes
connects epithelial cells to each other

49
Q

B-catenin

A

in nucleus as transcription factor or peripheral junction

50
Q

loss of e-cadherin

A

invasion
B-catenin leaves cell junction, moves to nucleus to act as proliferative transcription factors

51
Q

more e-cadherin/uvomorulin

A

limits cell invasion by contact inhibition
B-catenin at junction

52
Q

cadherin

A

transmembrane glycoprotein synthesized on rough ER that mediated Ca2+ adhesion

53
Q

tight junctions

A

adherins junctions form 1st
limit paracellular diffusion
composed of claudin
prevent EMT
connect/link to actin MF microfilaments
ZO-1 tethers cytoskeleton
belt-like

54
Q

claudin

A

composes Tight junctions

55
Q

adherens junctions

A

bind actin MF - cytoskeleton

56
Q

plasmodesmata

A

in plants; intercellular channels span cell walls and facilitate exchange of signaling molecules;
most similar to GAP junctions

57
Q

gap junctions

A

allow exchange

58
Q

integrins and cadherins

A

transmembrane proteins w a cytoplasmic domain connected to their cytoskeleton

59
Q

integrins

A

interact with ECM and actin cytoskeleton cytoplasmic domain.
growth factors stored in ECM can bind w integrins and activate proliferative signaling pathways and ECM invasion
cells gain function to invade assisted by focal adhesions and integrin dimers

60
Q

focal adhesions

A

integrin-ECM migration by actin polymerization

linked to the actin cytoskeleton

61
Q

anchorage dependent growth

A

grow attached to surface ECM as good neighbors

62
Q

Hayflick limit

A

telomere function and senescence limit doublings of cells

63
Q

retrotransposons

A

via reverse transcriptase from mRNA to DNA
NO introns

64
Q

EMT

A

invasion and metastisis
integrin activation increases cell adhesion to ECM

65
Q

integrin activation

A

increase cell adhesion and create focal adhesions linked to actin cytoskeleton

66
Q

barriers to MC

A
  1. cheaters - specialization
  2. nutrient transport by bulk flow
  3. adhesion by integrins
  4. communication by junctions
67
Q

snowflake yeast

A

mutation in cytokinesis = incomplete binary fission
clonal
heterogeneity in growth form from additional mutations
cost of MC overcome by specialization
MC phenotype has fitness advantage and maintained

68
Q

angiogenesis

A

hypoxia HIP1a by low O2 releases VEGF
terminated by Dll4 and PDGF

69
Q

invasion and metastisis

A

EMT by loss of uvomorulin/e-cadherin
integrin activation

70
Q

replicative immortality

A

telomerase constitutively overactivated

71
Q

sustain proliferative signaling

A

Ras jammed accelerator or activated EGF receptors by AKT or MAP/ERK kinase pathway

72
Q

resisting cell death

A

damage to TP53, mutated AKT

73
Q

pericytes

A

connect by integrins and gap junctions
stabilize new capillary

74
Q

AKT

A

protein blocks apoptosis (phosphorylation by kinases)

75
Q

evade growth suppressors

A

loss of TP53 or mutations or MDM2 overexpression, RB

76
Q

genomic instability

A

no cell cycle checkpoints, mutations damage DNA

77
Q

telomere shortening

A

senescence and apoptosis

78
Q

metabolism

A

warburg effect of glycolysis via HIF1a

79
Q

commensalism

A

1 benefits, 1 neutral

80
Q

ammensalism

A

negative from 1 pop onto other

81
Q

sprouting angiogenesis

A
  1. tip cell selection of high delta expression, low notch expression
  2. tip cell migration
  3. stalk elongation
  4. capillary fusion
  5. blood flow perfuses new capillary
  6. pericytes stabilize new capillary
82
Q

tip cell selection in angiogenesis

A

high delta expression, low notch

83
Q

diffusion

A

eletron transport chain
ficks 1st law

84
Q

axelrod

A

tumor progression facilitated by cooperation in form of by-product mutualism in genetically diverse tumor cells

85
Q

VEGF

A

angiogenesis
triggers tip cell formation
fibroblasts and endothelial cells bind VEGF
endothelial cells express Dll4 delta on surface
endothelial cells express notch on surface

86
Q

TME

A

cytoskeleton stiffens
non-cancer cells use alternative metabolic pathways
cancer cells avoid immune system

87
Q

actin

A

polymerize to form MF

88
Q
A