Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core II > S3 > Flashcards

S3 Flashcards

1
Q

dynamic instability

A

individual MTs do different things at different time (dont just grow at cc)
GTP cap
catastrophe
rescue

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

critical concentration for assembly

A

an amount at which there is enough in solution to polymerize
plus end has lower critical concentration than minus end - polarity
MTs also need GTP, 37 degrees, Mg

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

treadmilling

A

illusion of movement

one side grows while other side shrinks seen in vivo, not actual movement

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

selective stabilization

A

proteins can bind to lattice to prevent dissasembly - important for cell polariation
Tau, MAP. double cortin, STOP, plectin, etc

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

GTP hydrolysis and micrtotubules

A

all free tubulin is GTP-tubulin
adding to plus end forming GTP cap
then hydrolysis behind making GDP tubulin
catastrophe if GTP cap is lost,
rescue if cap comes back before dissasmbled
not technically necessary to form but without it cant dissassemble to do work

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

microtubule based molecular motor proteinsd

A 
get more work done than that stored in MTs
ATPase
dynein is retrograde toward minus end
kinesin is anterograde toward plus end
motor and cargo domain
processivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

tau

A

important for stabalizning MTs
absent in alzheimers
neruon specific

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

katanin

A

cuts microtubule by pulling tubulin through hexamer pore

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

microtubules

A 
tubulin subunits
hollow
polar
dynamic
highly conserved
railway for motor proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

actin filaments

A 
actin subunits
non holow
polar
dynamic
highly conserved
railways for motor protieints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

intermediate filaments

A 
various kinds of intermediate filament subunits
nonhollow
non polar
non dynamic
diverse
not a railway for motor proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MT subunits

A

alpha beta dimer

free tubulin dimers

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

MT polarity

A

alpha is minus end
beta is plus end
nothing to do with charge

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

mitotic vs interphase microtubule org

A

both have centrosomes with minus ends and plus ends out
but Interphase has one in the center going out
mitotic has 2 on oposite ends
‘centralized foci’

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

nucleation

A

getting new MTs started
has Lag without nucleation seed
less energetically favorable than elongation
needs MT nucleating elements to make favorable like centrosomes and basal bodies

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

nucleating sites

A

in pericentriole matrix PCM around centrioles
rings of gamma tubulin
centrioles themselves only source of extracellular MTs

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

cilia and flagella

A

short and long
9+2 arrangment
flagellar dyeinn
basal body is centriole that contacts cell membrane

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

gamma tubulin

A

gamma turc is ring for nucleation sites

unclear if it binds to alpha or beta but it helps make polar proto filament

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

cut and run

A

Mts break off centrosome then move for non centrosomal arrays like epithelial cells with apical and basal ends

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

coverslip movement

A

kinesisn walks toward plus end to MT moves in dirextion of minus
Dynein walks toward minus end so plus end leads

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

neuron MT patterns

A

dynien moves them into axon so plus end toward terminal

dendrite mixed because dynin moves in there then kinesins move it around

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

axon branch formation

A

katanin cuts and tau gets phosphorylated while it moves to new branch
spastin cuts and tau stays on MT chunks that move to new branch

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

actin filament growth and force on membranes

A

at cell concentrations actin is more stable in a filament so polymerization for brownian ratchet when it bends to allow another subunit then bends back working on the membrane

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

myosin force generation cycle

A

attached and nucleotide free

ATP binds mysosin so it releases actin

ATP hydrolysis to ADP.Pi bound cocks forward

Pi release ADP bound and bound to actin while cocked forward

ADP release so nucleotide free again and bends back moving actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

conservation of actin

A

highly conserved in eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

human actin isoforms

A

5
muscle - smooth, skeletal, cardiac
cytoplasmic - beta, gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

actin monomer

A

unusual subdomain structure
ATP binding sites
hydrolyzes and exchanges nucleotides slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

actin filament

A

polar
subdomain 2 into 1-3 cleft
ATP hydrolysis is fast ier in filament than in monomer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

in vitro actin assembly kinetics

A

nucleation slow and highly concentration dependent
elongation is fast and aysmetric - barbed + end is 1-3 cleft
pointed - end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

[actin]eq

A

a fixed value that is the balance of forward and revere reactions
the critical concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

buffering free actin

A

very little exists in cells
binds to beta-thymosin blocking both ends
most bins profilin which is a nucelotide exchange factor blocks elongation only on pointed end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

growth on barbed end

A

beta thymosin blocks both ends
prolifin allows barbed end addition
almost all elongation this way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

nucleation of actin

A

blocked by beta thymosin and or prolifin so nucleation is prevented in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

nucleation factors for actin

A

needed to allow filaments to grow in the right place at the right time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

actin elongation control

A

capping proteins to prevent elongation and depolarization like barbed end CapZ
elongation factors like formins, ENA/VASP control actin delivery and are capping protiens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

actin disassembly

A

ATP hydrolysis destabalizes the filament meaning that ADP actin dominates away from barbed end
severing factors generate new pointed ends
capping proteins will arrest growth at barbed end while the unpcapped pointy end depolymerizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

lamellipodia

A

branched arrray
broad flat rapidly polymerizying protuisions in 2d environments
densely branched actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

lamellipodia assembly and disassembly

A

nucleated by Arp2/3 complex at membrane
WASp/Scar proteins activate Arp2/3
growing filaments pus mesh away from membrane into cell
agin filaments are enriched by ADP actin and targetted for recycling by coflin
depolarized gets grabbed and recharged by profilin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

filopodia

A

parrallel bundled arrays
fast growing
nundling protein like fascin and a TIP complex
come from branched arrays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

actin crosslinking

A

different bundling proteins result in different structures
alpha-actin - anti-parallel bundling factor

usually told apart by distance btwn filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

myosin

A

actin binding motor

walks toward barbed end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

different myosin functions

A

same idea but differneent strucutre can be used for different cargo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

stress fibers

A

have focal adhesions of actin but look similar to muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

sarcomere

A

repeated in Skeletal muscle making it look striated

like a stress fiber with overlapping actin and myosin and caps instead of focal adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

skeletal muscle regulation

A

troponin is bound to tropomyosin which blocks myosin from binding to actin but Ca comes and removes troponin so tropomyosin moves so myosins can do its thing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

skeletal mucle triggering

A

t tubules send action potential

sarcoplasmic reticulume then releases Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

cell polarity

A

differences in shape and structure of cells

asymmetry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

regulated polarization

A

like lymphocyte becoming macrophage which is a direected homoestatic or immune response for migration and contact with other cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

T cells

A

2 poles and an axisl of polarity
migration
competition
asymmetric division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

epitheilai cells

A

polarized protein diestribution between basal and apical ends
apical has actin and cell cell junction
Par6, Par3, APKC on apical side of junction
uses gradents and transporters to have nutrients flow through
cell cell junction dilineate transporter types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

distribution of PAR proteins

A

Par3/Par6/aPKC
anterior side of asymmetric cell division
distal end of neve axon
leading end of cell migration
apical side of cell cell junction in epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

3 steps of cell migration

A

extension of leading edge
nuclear movement
tail contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

migrating cell adhesion

A 
extend
adhese
translocate
de adhese
focal adhesion kinase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

distribution in C elegans

A

Mex5/mex6
Par3/6/aPKC
all anterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

symmetric vs asymmetrci

A 
cadherin complex
zonular protein
apical marker/cadherin hole
if even amounts of above three then symmetrical
side with cadherin hole becomes NPC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

2 axis of polarity

A

apical-basal

planar cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

PCP mutants

A

disorginization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

division of neural progentior cells

A

vertically = 2 NPC

horizontal or angled = 1 NPC 1 neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Pro axon factors

A

PI3K
AKT
tau
PKB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

pro dendrite

A

PTEN

GSK-3 beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

planar cell polarity

A

2 axis: circunferential and radia
strucutres organs
downstream of wnt

62
Q

posterior c elegants

A

pie1
par1,2
p-granules

63
Q

wnt signaling

A

frizzled
disheveled
knock out experiments
gene transcription (canonical has beta catinin or calcium)
cytoskeleton remodeling for PCP has rho gtpase and JNK

64
Q

why are there size limits in microscopy

A

visible wavelength, resolution

65
Q

importance of tissue processing like fixation embedding sectioning

A

just to better visualize

66
Q

importance of specialized illumination

A

better visualize

67
Q

how to follow protein dynamics in living cells

A

fluroscence

68
Q

light vs electron vs atomic force microscopy

A

biggest to smallest

69
Q

compare images from atomic force microscopy, scanning electron microscopy, and transmission electron microscopy

A

d

70
Q

refractive index

A

ratio of light in a vaccuum to light through medium

used to match numerical aperture of a lens

71
Q

limits of resolution

A

minimum that can be achieved given the limitations of the medium used for microscopy and what is used to produce the image
defined by distinguishing btwn two objects

72
Q

photobleaching

A

overdoing the flourescence and destroying the flurophore

photoprotective scavengars help

73
Q

phototoxicity

A

hurting cells/samples by shining laser on i t

74
Q

deconvolution microscopy

A

math enhances images

75
Q

two photon microscopy

A

better than confocal

76
Q

fluorescence resononance energy transfer FRET

A

multiple dyes used to map interactions

77
Q

photoactivation

A

caged molecules remain unseen until catalytically freed

78
Q

total internal reflection fluorescence

A

TIRF
used to amplify from 2D coverslip
light bounces at an angle

79
Q

transmission electron m

A

shoots electrons through sampe to acheive 2 milllion x mag
wavelenght of electron is smaller than light
v inverse to w
ultra thin slicing

80
Q

scannning electron m

A

cover sample with metal and shoot with electrons

image based on scatter

81
Q

atomic force microscopy

A

bounce laser off of tip of probe
measure deviations
can see individual atoms

82
Q

visible light

A

0.4um to 0.7um

83
Q

meiosis vs mitosis

A

meisosis has two stages ending in 4 haploid cells

mitosis has its steps leading to 2 diploid cells

84
Q

meiosis I vs mitosis

A

homologus chromosomes connect and exchange parts

then pairs move to opposite sides

85
Q

APC/C

A

something to do with metaphase anaphase checkpoint

gets activated by cdc3- to help ubiquinate m cyclin-cdk and end metaphase

86
Q

Cdk activating kinase

and cyclin

A

get turned on by Cdc25 and off by wee1 kinase

different versions G,s, M m is for m phase

87
Q

phases of meisosis

A 
pro
meta1
ana 1
telo 1
pro 2
meta 2
ana 2
telo 2
basically 2 division: first pairs of homolougs then sister chromatids
88
Q

prophase I

A

homologuous recombination

crossing over synaptonemal complexl

89
Q

synaptonemal complex

A

combines two homologs with cohesisn and transverse filaments

90
Q

cohesin

A

4 units making a ring around sister chromatids

scc3-scc1 hook gets cleaved in anaphase

91
Q

homologous recombination

A

homologous dna exchange parts
for repair
accurate separation because chiasmata between correct homo pairs
genetic diversity

92
Q

chiasmata

A

happens after cross over when physically linked still

93
Q

HR deficient

A

fail to form SC and dont get cross overs

94
Q

separase in meiosis I

A

releases cohesin along the arms but cohesin near centromere is intact

95
Q

nondisjunction

A

no crossover - unstable and random
distal cohesion - unstable and random
proximal crossover - reductional division in meisosi II (stuck)
so crossovers cant be random but must be medial

96
Q

cross over interference

A

good thing?
two or more crossovers happen, so adjacnet events are located furthera apart than expected from random
but protects chiasmata

97
Q

When can DSB happen

A

prophase I

98
Q

spo11

A

catalyzes double strand breaks
part of large complex
so phosphorylation of Mer2 upregulates it

99
Q

double strand break recombination model

A 
resection
strand invation (Rad51)
synthesis
capture second end
synthesis
double holliday junction intermediate
cut both for resolution and either have crossover or non crossover
100
Q

synthesisi dependent strand annealilng

A

syn
dissociat
anneal
get non crossover

101
Q

Non crossover resultes

A

DSBR fits a lot but non crossovers appear at wrong time so maybe SDSA makes those

102
Q

mitotci spindle

A

astral MTs
kinetochore MTs
interpolart MTs

103
Q

astral MTs

A

stabalize centrosome

104
Q

kinetochore

A

connect centrosome to homo

105
Q

interpolar

A

stabalize entresomes to each other

106
Q

3 stages of apoptotici cell removal

A

find me
eat me
anti inflammatory cytokines

107
Q

procaspase activation

A

inactive procaspases have 2 celaveage sites
cleaveage activated by other active caspase so cascade
then dimerize

108
Q

fas ligand model

A

extrinsic apoptotic pathway
fas ligand on killer lymphocyte binds to Fas death receptor leading to association of fas-associated death domain FADD and assembly of Death inducing signaling complex DISC which activates procaspase 8,10
death effector domain DED
Caspase activating and recruiting domain CARD

109
Q

cytocrhome c

A

apoptotic stimulus relases from mitochondria
cc activates apaf1 (apoptotic protease activating factor)which has CARD domain and multimerizes to apoptosome
recruites procaspase 9 which gets executioner caspases

110
Q

activation of intrinsic pathway

A

apoptotic stimuli like BH3 inactivates the anti-apoptotic Bcl2 protein allowing BH123 to dimerize on outermembrane of mito so cc can get out

111
Q

scheme of mitochondria

A

basically bax/bak open a pore casuing cc and then mDNA to fall out

112
Q

increased production of Bcl2 protein

A

after a survivial factor activates a receptor, transcription is upregulated making more bcl2 to block apoptosis

113
Q

inactivation of proapoptotic BH3 only bcl2 protein

A

survival activates receptor activating AKt kinase whichactivates Bcl2 and inactivates Bad
blocking apoptosis

114
Q

inactivation of IAPs

A

survival factor and receptor

MAP kinase inactivates Hid which activates IAPs which i think block cc

115
Q

inflammosome

A

causes inflammation kinda like DISC in apoptosome
ASC or apoptis asssociated speck like protein containing a caspase recruitment
activated by toxins to mobilize immune system, caspase 1 releases cytokines to recruit the A team
NALP3 and IPF3 are variants

116
Q

necroptosis

A

causes immune response
necrosome with RIP3 kinase, caspase 8 activates
death from membrane osmolysis, energetic catastrophe, lipid peroxidation

117
Q

start/restriction point

A

when cells decide to go from G1 to S

118
Q

cyclin dependent kinase

A

depending on type of cyclin, will activate CDK for M or S phase

119
Q

G1-CDK

A

cyclin D

cdk4, cdk6

120
Q

G1/S-CDK

A

cyclin E

cdk2

121
Q

S-Cdk

A

Cyclin A

Cdk2,cdk1

122
Q

M-CDK

A

cyclin B

Cdk1

123
Q

regulation of CDK

A

transcription
+/-p
Cdk inhibitors
ubiquitind dependent proteolysis

124
Q

+/-P of Cdk

A

CAK cdk activating kinase
Wee1 +P inhibits
Cdc25 -P activates

125
Q

Cdk inhibitors

A

p16, p21, p27

bind to an inactivate the active cyclin-cdk complexes

126
Q

ubiquitin dependent proteolysis

A

APC/C: Anaphase-promoting complex/cyclosome: ubiquitin ligase complex
gets turned on by Cdc20 which tags cyclin B for degredation to make meta to ana transition

127
Q

SCF

A

Skp1-cullin-f-box ubiquitin ligase complex

tags a Cdk inhibitor to promote S phase entry

128
Q

S phase

A

DNA replication

sister chromatid cohesion

129
Q

M phase

A

mitosis

cytokinesis

130
Q

licensing factors

A

Cdc6
Cdt1
make sure chromosome duplication happens once only

131
Q

prophase

A

chromosome condensation
kinetochore
two centrosomes already

132
Q

prometaphase

A

nuclear envelope breaks down
mitotic spindle forms
centrosome at spindle poles

133
Q

metaphase

A

chromosomes are attached to spindle MTs at kinetochore

MTs line up signaling Met-anaphase transition

134
Q

anaphase

A

sister chromatid separation

135
Q

Telophase

A

chromosomes arrive at poles
chromosome decondensation
nuclear envelope reassembles
contractile ring starts to contract

136
Q

cytokinesis

A

contractile ring creates cleavage

telophase steps complete

137
Q

which Cdk starts mitosis

A

M-CDK

Cdk 1 and m-cyclin

138
Q

condensin

A

protein for prophase condensation of chromosomes

139
Q

breakdown of nuclear envelope

A

M-Cdk

140
Q

parts of mitotic spindle

A

spindle poles
astral microtubules
kinetochore microtubules
interpolar microtubules

141
Q

spindle poles

A

centers of microtubule nucleation with minus ends

142
Q

astral MTs

A

radiate outward from the poles and contact the cell cortex to help position MS

143
Q

kinetochore MTs

A

attach sisters at kinetochores

144
Q

interpolar MTs

A

+ ends overlap making antiparallel array

145
Q

centrosome duplication

A

G1/S-CDK
centrioles separate
act as templates
dont spread and duplicate until M phase

146
Q

tension check

A

auroro B kinase phosphorylates Ndc80 when low tension and increases affinity for MT plus end so it can get pulled away

147
Q

APC/C and separation

A

ubiquinates securin freeing separaste to cleave cohesin to separate sister chromatids

148
Q

if choromosomes not properly attached to MS

A

Mad2 binds APC/C and inhibits so no separation

149
Q

RhoA GTPase

A

assembly and contraction of contractile ring which uses actin and myosin II

150
Q

extracellular promoters

A

mitogens - mitogen receptors
growth factors - RTKs and mTOR
survival factors

151
Q

extracellular suppressors

A

Stress

apoptotic signals

Core II (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions