final Flashcards

1
Q

what gives actin filaments polarity

A

actin filaments have same polarization give polarity

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2
Q

how are MF dynamic

A

by assembling/ itself

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3
Q

is actin an atpase

A

yes

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4
Q

what reflects polarity of MF

A

more rapid addition of G actin at the positive end

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5
Q

what happens after G actin monomers are assembled

A

the ATP bound to them is hydrolyzed

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6
Q

where is ATP actin in MF

A

growing end

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7
Q

where is ADP actin on MF

A

most of MF (not growing end)

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8
Q

where is there an increased rate of polymerization in MF

A

positive end

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9
Q

what is tread milling

A

monomers are continuously added to the positive end and removed at the negative end

leaving it same length

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10
Q

what kind of cells have lamellipodia and filopodia

A

crawling cells

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11
Q

what regulates organization and behaviour of MF inside a cell

A

actin binding proteins

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12
Q

how do actin binding proteins work

A

sequester monomers to regulate rate pf polymerization

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13
Q

what does availability of ATP bound G actin affect

A

MF assembly

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14
Q

what are 3 actin binding proteins

A

thymosin Beta 4

profilin

cofilin

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15
Q

what does Thymosin beta 4 do

A

binds to ATP actin monomers and prevents them from polymerizing

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16
Q

what does profilin do

A

binds to ADP G actin and catalyzes the exchange of ADP for ATP

promoting polymerization

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17
Q

what does cofilin do

A

binds to ADP actin in a MF severing it and promoting depolymerization

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18
Q

are actin binding proteins can cap actin filaments

A

yes

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19
Q

does whether an MF can grow depend on wither their filament end his capped

A

yes

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20
Q

what are 3 actin binding proteins that cap the ends

A

capping proteins

Cap Z

Tropomodulins

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21
Q

what do capping proteins do

A

bind the ends of a filament to further loss/gain of subunits

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22
Q

what does Cap Z do

A

binds to + end to prevent addition/loss of subunits

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23
Q

what does tropomodulins do

A

binds to - ends preventing addition/loss of subunits

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24
Q

can actin binding proteins sever actin filaments

A

yes

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25
Q

what are actin binding proteins that sever to actin filaments

A

gelsolin

cofilin

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26
Q

what does gelsolin do

A

breaks actin MFs and caps the newly exposed + ends, preventing further polymerization

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27
Q

what does cofilin do

A

filament severing protein

facilitates depolymerization

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28
Q

what kind of protein is actin

A

globular

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29
Q

what kind of actins are muscle specific

A

alpha actins

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30
Q

what happens once an actin is synthesized

A

folds into a globular u shaped protein that can bind ATP/ADP

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31
Q

what kind of actins are muscle specific

A

beta actins

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32
Q

what does G actin (globular actin) polymerize to form

A

MF (F-actin)

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33
Q

can actin binding proteins regulate monomers and the rate of polymerization

A

yes

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34
Q

what actin binding protein regulate monomers and the rate of the polymerization

A

formins

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35
Q

what do formins do

A

control assembly of actin filaments in vivo

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36
Q

what proteins cross link filaments

A

actin binding proteins

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37
Q

Why do filaments cross link

A

resist mechanical pressure

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38
Q

what actin binding protein helps filaments cross link

A

filamin

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39
Q

what kind of protein bundle actin filaments

A

actin binding protein

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40
Q

what kind of actin is prominent in actin filament bundles

A

alpha actin

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41
Q

why is actin bundled into filaments

A

enhancing rigidity

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42
Q

what link MFs to membranes

A

actin binding proteins

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43
Q

what nucleate new actin filaments

A

actin binding proteins

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44
Q

what are the most stable and least soluble cytoskeletal components

A

intermediate filaments

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45
Q

what kind of filament is keratin

A

intermediate

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46
Q

what is the major difference between MF/MT and IF

A

IFs can be made of many different proteins

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47
Q

what is the largest component of the cytoskeleton

A

MTs

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48
Q

what do MF hydrolyze

A

ATP

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49
Q

what do MT hydrolyze

A

GTP

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50
Q

what do IFs provide

A

mechanical strength to tissues

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51
Q

what are the main roles of each cytoskeletal component

A

MT: resist bending when a cell is compressed

MF: serve as contractile elements that generate tension

IF: elastic and withstand tensile forces

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52
Q

what are the supporting structures of nucleus

A

nuclear matrix and nuclear lamina

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53
Q

what does a nuclear matrix do (nucleoskeleton)

A

insoluble fibrous network that helps maintain nuclear shape

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54
Q

what does a nuclear lamina made of

A

thin dense meshwork of fibres

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55
Q

what kind of motor is kinesin

A

anterograde MT motor

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56
Q

what kind of motor is dynein

A

retrograde MT motor

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57
Q

what is cell contractility

A

shortening of muscle cells

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58
Q

what are the 2 eukaryotic motility systems

A
  • interactions between MT and motor proteins (kinesins and dyneins)
  • interactions between actin mF and myosin
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59
Q

what do motor proteins do

A

convert chemical energy to mechanical energy

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60
Q

what are the 3 motor proteins (and MT or MF)

A

kinesins - MT

Dyneins - MT

Myosins - MF

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61
Q

do any motor proteins use IF tracks

A

no

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62
Q

what do motors undergo cycles of

A

ATP hydrolysis and release of ADP and Pi and aquisition of new ATP molecule

63
Q

what subjects motor proteins to friction

A

viscous cytosol

64
Q

what are the 2 types of MT

A

cytoplasmic MT

Axonemal MT

65
Q

what is an axoneme

A

central shaft of cilia and flagella

highly ordered bundle of Mts

66
Q

what direction is force generated with flagella

A

parallel

67
Q

what do MT provide

A

rigid set of tracks for transport of organelles/vesicles

68
Q

what direction is inbound and outbound

A

towards - is inbound

towards + is outbound

69
Q

what provides force needed for movement

A

Mt associated motor proteins that walk along MT

70
Q

what direction is anterograde axonemal transport

A

towards + end (away from centrosomes)

71
Q

what direction is retrograde axonemal transport

A

moves cargo towards - end

72
Q

what is special about kinesin 14 family

A

are - end directed

73
Q

what is similarity and difference between kinesins and dynein

A

move similar materials in opposite directions

74
Q

what direction of force is generated by cilia

A

perpendicular

75
Q

what causes MT sliding

A

axonemal dynein

76
Q

what allows cilia and flagella to bend

A

MT sliding

77
Q

what are primarily used in sensory structures

A

cilia

78
Q

what are the two types of myosins

A

unconventional

conventional (type 2)

79
Q

what direction do myosin move

A

most move towards the + end

type 6 is exception

80
Q

what does a muscle fibre consist of

A

long thin multinucleated cell that contain many myofibrils divided into sarcomeres

81
Q

what are sarcomeres

A

fundamenta contractile unit of muscle cell

82
Q

what are sarcomeres composed of

A

thick filaments: staggered arrays of myosin 2

thin filaments: actin MFs with other bound proteins

83
Q

what are thin filaments made of

A

tropomyosin:

troponin

84
Q

what is troponin composed of

A

3 polypeptides

TnT
TnC
TnI

85
Q

what constitute a calcium sensitive switch in sarcomeres

A

tropomyosin + troponin

86
Q

what does tropomodulin

A

caps the - ends of the filaments to maintain stability

87
Q

what does cap Z do

A

caps the + ends and attaches the MF to the Z line

88
Q

what does the nebulin do

A

stabilizes and binds the thin filament ti the Z line

89
Q

what does alpha actin do

A

cross links the z line to the MF keeping the thin filaments parallel

90
Q

what does myomesin do

A

bundles myosin molecules

91
Q

what is titin do

A

attaches the thick filaments to the Z lines and keeps thick filaments in the correct position relative to thin filaments during contractions

92
Q

what is the sliding filament model

A

muscle contraction is due to thin filaments sliding past thick filaments with no change in length of either

93
Q

what happens in the sliding filament model

A

myosin walks towards + end od the actin MFs (thin filaments)

because the + end is anchored at the Z line

the movement of myosin pulls actin filaments towards center

= contraction

94
Q

what happens to cross bridges during contractions

A

they form and dissociate rapidly

95
Q

what is chemotaxis

A

directional movement in response to graded chemical stimulus

96
Q

what are chemoattractants

A

cells move towards a higher concentration of the diffusible molecules

97
Q

what is a chemorepellent

A

cells move towards a lower concentration of the diffusible molecules

98
Q

what happens in G0 phase

A

resting

99
Q

what happens in g1 phase

A

cell growth. normal metabolism, organelles duplicate

100
Q

what happens in S phase

A

DNA replication and chromosome duplication

101
Q

what is G2 phase

A

cell grows and prepares for mitosis

cells contain twice the number of chromosomes

102
Q

what happens in mitosis

A

segregate copies into 2 daughter cells

when cells actually divide

103
Q

does nuclear division (mitosis) or cytoplasm division (cytokinesis) happen first

A

mitosis

104
Q

what happens in prophase

A

chromosomal material condenses into chromosomes

cytoskeleton is disassembled

mitotic spindle is assembled

golgi and ER fragment

nuclear envelope disperses

105
Q

what happens in prometaphase

A

chromosomal MT attach to kinetochores

chromosomes are moved to spindle equator

106
Q

what happens in metaphase

A

chromosomes are aligned along the metaphase plate

107
Q

what happens in anaphase

A

centromeres split

chromatids separate

chromosomes move to opposite spindle poles

108
Q

what happens in telophase

A

chromosomes cluster at opposite spindle poles

nuclear envelope assembles around chromosome clusters

golgi and ER reform

daughter cells are formed nu cytokinesis

109
Q

what does a ligand receptor interaction results in

A

conformational change

110
Q

what are the 3 classes of signalling molecules

A

endocrine: produced far from target (reach via circulatory system)

paracrine: diffuasable and act locally or over short range via extracellular fluid

autocrine: act on the same cell that produces it

111
Q

what are eicosanoids

A

fatty acids that regulate pain, inflammation, blood pressure, blood clotting

112
Q

are most signalling molecules hydrophobic or hydrophilic

A

hydrophobic

113
Q

what are 3 main classes of cell surface receptors

A

G protein coupled receptors

enzyme linked receptors (RTK)

ion channel linked receptors

114
Q

what is the dissociation constant (kd)

A

the concentration of free ligands needed to produce a state in which half the receptors are occupied

115
Q

what are agonists

A

drugs that activate the receptor they are bound to

116
Q

what are antagonists

A

drugs that bind receptors without activating it

blocking it

117
Q

what are second messengers

A

some effectors generate small molecules or ions that relay signals from one location to another

118
Q

what do kinases do

A

phosphorylate

119
Q

what do phosphatases do

A

dephosphorylate

120
Q

what does phosphorylation do

A

changes a proteins charge and often leads to a conformational change which alters ligand binding (increasing/decreasing activity)

121
Q

what happens to signal in divergence

A

one signal leads to effects on multiple pathways

122
Q

what happens to signal in convergence

A

signals from multiple ligands/receptors activate same pathway

123
Q

what happens to signal to crosstalk

A

signals from different pathways can affect components of multiple pathways

124
Q

do cells sense fixed concentrations or changes in ligand concentrations

A

changes

125
Q

what happens in receptor mediated endocytosis (signalling)

A

cells reduce density of receptors on their cell surfaces

126
Q

what is a common method of desensitization

A

phosphorylation

127
Q

what kind of G protein associates with GDP/GTP molecules

A

alpha G protein

128
Q

what is desensitization

A

cells stop responding to the stimulus despite continued presence of the stimulus

129
Q

what G protein is associated with K+ channel

A

G beta gamma

130
Q

what causes signal termination

A

arrestin

131
Q

what does receptor mediated endocytosis

A

removes targeted receptor from cell surface

132
Q

what is cyclic AMP (cAMP) from

A

from cytosolic ATP by adenylyl cyckases, and enzyme anchored in the plasma membrane

133
Q

what does phosphodiesterase do

A

degrades cAMP

134
Q

what is the main target of cAMP

and what happens

A

protein kinase A (PKA)

acts as allosteric activator

regulates the separation of the regulatory and catalytic subunits

135
Q

what does activation of kineases allow for

A

a significant level of signal amplification

136
Q

what stimulates the inactivation of the enzyme system responsible for synthesis of glycogen

A

cAMP

137
Q

what drives most of the effect of cAMP

A

PKA

138
Q

what do AKAPs provide

A

scaffolding for coordinating protein-protien interactions by sequestering PKA to specific cellular locations

139
Q

what happens to PKA when cAMP levels rise

A

PKA is activated

140
Q

what does activation of phospholipase C trigger

A

cleavage of PIP2

which generates IP3 and DAG

141
Q

what can lipids cleaved from membranes be used for

A

second messengers

142
Q

why are cytoplasmic Ca2+ concentrations are maintained at low levels because

A
  • Ca2+ channels in SER are kept closed
  • Na+/Ca2+ antiporters and calcium ATPases in plasma membrane and SER actively transport Ca2+ out of cytosol
143
Q

how can signalling lead to to increased cytosolic Ca2+ concentrations

A

voltage gated Ca2+ channels can be opened by nerve impulses

IP3 receptor channels (ligand gated Ca2+ channels) can open upon IP3

Ryanodune receptor channels (ligand-gated Ca2+ channels) are sensitive to calcium ( calcium induced calcium release)

144
Q

what is G protein bound to when on/off

A

on : GTP

off: GDP

145
Q

what do GAPs regulate

A

GTPases activating proteins

146
Q

what do GDIs regulate

A

Guanine nucleotide dissociation inhibitors

147
Q

what do GEFs

A

Guanine nucleotide exchange factors

148
Q

what are the monomeric G proteins and what do they relate to

A

Ras - signal transduction
Ran - nuclear transport
Rab - tethering vesicles
Sar 1- vesicle formation

Rho - actin-binding protein regulator

149
Q

what is Ras-MAP activated by

A

when a growth factor (EGF) binds the extracellular domain of RTK

150
Q

what does Ras-GTP have a high affinity for

A

kinase Raf

151
Q

what are 2 main domains in nuclear receptors

A

ligand binding domain

DNA binding domain

152
Q

what is the starting material for synthesis of steroid hormones

A

cholesterol

153
Q

what mediate the opening of Na+ channels

A

neurotransmitters