cells final Flashcards

(88 cards)

1
Q

HeLa cells immortality

A

overactive telomerase never shortens allowing indefinite replication and division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

gene regulation

A

chem modifications to chromatin and histones, during transcription or translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

chromatin

A

dna, rna, proteins packed to give chromosome shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RNA processing

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

srRNA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HAT

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

+ control lac operon

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • control lac operon
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

controls cAMP levels in lac operon

A

rate of bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

high lactose and high glucose lac operon

A

induced and inactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

negative cell cycle regulators

A

p53, p21, Rb tumor suppressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

positive cell cycle regulators

A

cyclin CDK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

EGF binding

A

Upregulating proliferation
Down regulating apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ZO-1

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

qRT-PCR

A

dna expression; further left = more transcription/translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

separation experiments

A

TLC, centrifugation, electrophoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

siRNAs

A

knock down gene in experiments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

silencing

A

repress transcription by change gene dosage and rate of transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

proximate

A

mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ligand

A

signaling molecule binds to receptor causes activating change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

membrane composition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pulse chase

A

trafficking and movement proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
evolution
by natural selection reqs variation that is heritable and results in differential reproductive fitness success
26
protein destined for ion channel
amino-terminal and signal anchor peptide seq
27
rough ER
studded w ribosomes; protein synthesis destined as transmembrane, secreted out, or lumen organelles default is secretion COP II move from ER to golgi
28
lysosomal enzymes
vesicles that break down protein; synthesized on rough ER, processed in golgi
29
Golgi apparatus
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
30
COP I vesicles
move golgi to ER
31
COP II
move ER to golgi
32
ER resident proteins
amino terminal sequence
33
amino terminal sequence
ER (lumen) proteins, ion channel protein, secreted rough ER
34
Coat proteins
make vesicles
35
destined for mitochondria/chloroplast, ER, secretion
amino terminal signal sequence
36
SRP
signal recognition particle is rna-protein complex
37
no signal peptide
free ribosome in cytosol
38
Sar I GTPases
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
GTPases
on or off protein switches regulate cell responses to EC signals cause cell survival, proliferation in nucleus to start transcription and gene expression
40
Ras
GTPase activates RAF kinase and MEK/MAP growth signal kinase and ERK/MAP activated by EGFR to cause cell proliferation
41
signaling molecule
polar ligand on cell surface like EGF
42
MDM2
degrades p53 (- regulator, ubiquinates)
43
p53
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
Rb
tumor suppressor binds to transcription factors and genes NOT transcribed
45
life history characteristics
lifespan litters/year reproductive age maturity # offspring parental care
46
(hemi)desmosomes
bind to IM filaments and connect w integrins Integrins and hemidesmosomes bind to ECm basal lamina
47
desmosomes
adhesive junction for mechanical stress stability containing cadherins
48
e cadherin
uvomorulin desmosomes connects epithelial cells to each other
49
B-catenin
in nucleus as transcription factor or peripheral junction
50
loss of e-cadherin
invasion B-catenin leaves cell junction, moves to nucleus to act as proliferative transcription factors
51
more e-cadherin/uvomorulin
limits cell invasion by contact inhibition B-catenin at junction
52
cadherin
transmembrane glycoprotein synthesized on rough ER that mediated Ca2+ adhesion
53
tight junctions
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
claudin
composes Tight junctions
55
adherens junctions
bind actin MF - cytoskeleton
56
plasmodesmata
in plants; intercellular channels span cell walls and facilitate exchange of signaling molecules; most similar to GAP junctions
57
gap junctions
allow exchange
58
integrins and cadherins
transmembrane proteins w a cytoplasmic domain connected to their cytoskeleton
59
integrins
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
focal adhesions
integrin-ECM migration by actin polymerization linked to the actin cytoskeleton
61
anchorage dependent growth
grow attached to surface ECM as good neighbors
62
Hayflick limit
telomere function and senescence limit doublings of cells
63
retrotransposons
via reverse transcriptase from mRNA to DNA NO introns
64
EMT
invasion and metastisis integrin activation increases cell adhesion to ECM
65
integrin activation
increase cell adhesion and create focal adhesions linked to actin cytoskeleton
66
barriers to MC
1. cheaters - specialization 2. nutrient transport by bulk flow 3. adhesion by integrins 4. communication by junctions
67
snowflake yeast
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
angiogenesis
hypoxia HIP1a by low O2 releases VEGF terminated by Dll4 and PDGF
69
invasion and metastisis
EMT by loss of uvomorulin/e-cadherin integrin activation
70
replicative immortality
telomerase constitutively overactivated
71
sustain proliferative signaling
Ras jammed accelerator or activated EGF receptors by AKT or MAP/ERK kinase pathway
72
resisting cell death
damage to TP53, mutated AKT
73
pericytes
connect by integrins and gap junctions stabilize new capillary
74
AKT
protein blocks apoptosis (phosphorylation by kinases)
75
evade growth suppressors
loss of TP53 or mutations or MDM2 overexpression, RB
76
genomic instability
no cell cycle checkpoints, mutations damage DNA
77
telomere shortening
senescence and apoptosis
78
metabolism
warburg effect of glycolysis via HIF1a
79
commensalism
1 benefits, 1 neutral
80
ammensalism
negative from 1 pop onto other
81
sprouting angiogenesis
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
tip cell selection in angiogenesis
high delta expression, low notch
83
diffusion
eletron transport chain ficks 1st law
84
axelrod
tumor progression facilitated by cooperation in form of by-product mutualism in genetically diverse tumor cells
85
VEGF
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
TME
cytoskeleton stiffens non-cancer cells use alternative metabolic pathways cancer cells avoid immune system
87
actin
polymerize to form MF
88