TEST 3 Flashcards
(94 cards)
1
Q
signal transduction
A
converting one form of information into another form
2
Q
the types of cell to cell communication
A
endocrine-through blood stream/organism wide- uses hormones
paracrine-local -uses a local mediator
autocrine-to itself -local mediator released out of cell then recieved by the same cell
neuronal-from neuron to neuron- neurotransmitters
contact dependant -physical features and receptor
3
Q
types of extracellular signal molecules
A
proteins/peptides/aminoacids nucleotides sterioids fatty acid derivitaives gases
4
Q
horomones
A
insulin
cortisol
adrenalin
testosterone/estrogen
5
Q
Local mediators
A
NO-gas
histamine
Nerve, Epidermal, Platelet Growth factors
6
Q
Neurotransmitters
A
acetylcholine and GABA
7
Q
Contact dependant
A
delta
8
Q
2 types of signaling molecules
A
small easily diffused across membrane molecules- these bind to receptors inside the cell
large not easily diffused across membrane molecules- these bind to receptors on the membrane of the cell
9
Q
signal molecules do what to different tissues
A
they affect different tissues differently ex- acetylcholine heart faster mouth-salivate muscles- contract
10
Q
how can combos of singaling molecules affect cells
A
different combos evoke different reactions from the target cell such as
- survival
- growth
- differentiation
- none=death
11
Q
cell responce times to signal molecule
A
can be fast or slow
- fast affects the present proteins in the cell to act in a certain way
- slow can affect altered protein synthesis and how the whole cell works eg cell growth
12
Q
pathway of signal molecule changing cell behavior
A
receptor
intracellular signaling molecules
effector proteins- which then make the change
then the target response (altered metabolism, shape, gene expression)
13
Q
functions of intracellular signaling pathway
A
relay signal onward through process of altering cell
detect other signals and integrate them
distribute signal to more effector proteins-complex response
take part in feedback loop to terminate or amplify
14
Q
proteins that add phosphate groups
A
kinases- serine/threonine/tyronsine
15
Q
proteins that remove phosphate groups
A
phosphatases
16
Q
how do phosphates act as a switch on proteins
A
the protein is first in a normal state
a signal is received which activates a kinase to turn ‘on’ the protein
the protein continues the signal onward
the protein is the turned ‘off’ and goes back to its normal state
17
Q
GTP signaling acting as switch
A
GDP is bound to off protein
signal comes in and GDP is switched out for GTP which turns ‘on’ protein
signal is put out by protein
phosphate leaves in the process going back to original state
18
Q
trimeric vs monomeric G proteins
A
mono- 1 protein
tri- 3 proteins
19
Q
3 cell surface receptors & examples
A
ion channel couple receptors- muscle receptors to acetylcholine
g protein couple receptors-heart receptors to acetylcholine
enzyme coupled receptors-
20
Q
substances that alter physiology by interacting with receptors
A
nicotine
heroin
benzos
21
Q
signal transduction by ion channel receptors
A
transmitting an AP across synapse
these are opened by neurotransmitters letting in ions which creates another AP
22
Q
structure of GPCR
A
7 alpha helixs across the membrane
GCPRS that bind to small molecules bind deep within the helixs forming a
pocket
GCPRS that bind to large molecules have large extracellular domains which
bind to the ligand
23
Q
what molecules bind to a GCPR
A
horomones, local mediators, neurotransmitters, proteins, peptides, fatty acids, amino acids
24
Q
GCPR
A
Gprotein couple receptors
25
composition of a g protein
3 subunits, alpha beta and gamma
when activated, the alpha switches GDP for GTP which separates alpha from
beta and gamma complex
once separated each complex can bind to target proteins in the cell which
relay the signal into the cell
the longer the subunits are bound to a target protein the longer the the relay
signal will be
26
how does cholera affect g proteins
cholera multiplies in the gut
in the gut it alters affect cells G proteins by stopping the alpha subunit from
hydrolyzing it GTP leaving the cell signal continuously open
this forces and out pour of water and Cl- into the gut forcing massive diarrhea
which leads to death
27
pertussis affect on g proteins
whooping cough gets into lungs and alters the alpha subunit of the g protein
which locks the alpha unit into its deactivated state
this stimulates coughing
28
speed of response of g protein affecting an ion channel vs membrane bound enzyme
responce of g protein on ion channel is immediate- when the g protein opens up into 2 separate complexs the beta/gamma complex slides into the ion channel which opens it
29
speed of response of g protein affecting an ion channel vs membrane bound enzyme
response of g protein on ion channel is immediate- when the g protein opens
up into 2 separate complexs the beta/gamma complex slides into the
ion channel which opens it
responce of g protein on membrane bound enzyme is slower- creates more
intracellular signalling moelcules which creates others and others
which can have different functions
30
most frequent class of enzyme & second messengers produced targeted by g protein
adenylyl cyclase- cyclic AMP
phsopholipase C- inositol triphosphate and diacyglycerol
31
how Cyclic AMP is made from g protein activation
when the alpha g protein activates and binds to adenylyl cyclase, it activates it
this creates more cyclic AMP from ATP, usually a cyclic AMP
phosphodiesterase undoes this work back to a normal AMP
32
how does caffeine work
caffeine inhibits the work of cyclic AMP phosphodiesterase, which usually
inhibits the work done by adenyly cyclase which creates the cyclic AMP
the adenyly cyclase is activated by g proteins
basically it stops the cAMP from being degraded which increases cAMP levels
33
cyclic AMP's fast vs slow ways to affect cells
fast- the activation of a g protein activates adendyly cyclase, this creates
massive amounts of cyclic AMP which activates an enzyme called AMP- dependent protein kinase (PKA), this activates a phosphoylation kinase which activates a glycogen phosphylase, which stimulates glycogen breakdown which creates energy for the cell very fast
slow- PKA phosphoylates transcription regulators which changes how genes are expressed, this can take minutes to hours
34
what does adenylyl cyclase make
cyclic AMP
35
what does phsopholipase C make
inositol triphosphate and diacyglycerol
36
phospholipase C second messenger actions
creates inositol phospholipid, which then opens the calcium channels in both
the plasma membrane and ER membrane which increases CA2+ levels
in the cell
also activates protein kinase C (PKC) needs to bind to Ca2+ to be active, which
phosphorylates other proteins
37
processes triggered by Ca2+
growth of embyo
muscle contraction
secretion in synapses
38
how cells stop Ca2+ ion signal, and how cellular levels are low
the calcium pumps both keep the cell levels low of Ca2+ and terminate the signal by them
39
how does calmodulin continue the Ca2+ signal
the protein calmodulin binds to Ca2+ conformationally, which allows it to bind to other proteins altering their activities
one example is when it does this with Cam Kinases in the brain which helps
learning
40
creation of NO and how it relaxes muscles
the blood vessel is lined with endothelial cells and smooth muscle cells
when acetylcholine is received by the endothelial cells, the cells create NO
which diffuses into the nearby smooth muscle cells relaxing the muscle
dilates blood vessel
41
why can NO only be used as a paracrine signal
as the gas diffuses, it runs into oxygen and water which converts NO into nitrates and nitrites in seconds
42
how do GCPRs transmit light fast through the retinas
in rods, light is sensed by GCPR rhodopsin, this activates g protein transducin which actvates a cascade of intracellular signaling which causes cation cahnnels to close in the membrane, this charges the membrane which laters neurotransmitter release which leads to a nerve impulse in the brain
43
how do cascades of photoreceptors allow us to adjust our eyes to dim/bright light
when lights are dim, intracellular cascade amplification is enormous, due to the
limited amount of light present
when lights are bright, intracellular cascades are super small, this depends on negative feedback to decrease Ca2+ which limits amplification
44
Enzyme coupled receptors
transmembrane protein with ligand binding domains on outer surface
cytosolic side can act as enzyme itself of forms a complex with a protein to act as enzyme
usually only 1 alpha helix across membrane
when bound to signaling molecule, it binds to another enzyme coupled
receptor with a signaling molecule, which brings the 2 intracellular tails
together activating their kinase domains
when this happens the two cytosolic tails get phosphorylated which then
allows proteins to bind to the tails which activates intracellular signaling
proteins
45
how do enzyme coupled receptors terminate signalling
tyrosine phosphates, removed the phosphates which the intracellular signaling proteins bind to
or
they are dragged into the cell and destroyed by lysosomes
46
what signaling molecules are activated by RTKs
```
phospholipase C (functions in the same way as GPCR ones)
RAS
```
47
RAS
small monomeric GTPase that is activated by an RTK to continue transmisssion of a signal
usually activates 3 MAP kinase modules first the kinase kinase kinase, then the kinase kinase, then the kinase
48
how does RAS create cancer
unable to stimulate GTPase activity, which leaves RAS continually turned on
this promotes uncontrolled cell proliferation
49
3 proteins of cytoskeleton
intermediate filaments
microtubules
actin filaments
50
intermediate filaments
fibrous proteins, 10nm, built like a steel cable/rope, of many small alpha helixes that are intertwined proteins
built to withstand stress of stretching
found in cytoplasm, surrounds nucleus/plasma membrane forming nuclear lamina
noncovalent, strength comes from overlapping lateral interations\
51
microtubules
hollow cylinder, made up of Tubulin, concentric circles layed on top of each 25nm
grows out of centrosomes near center of cell
during mitosis it dissasembles then reassembles as the mitotic spindle
can make up cillia and flagella
tubulin is made up of alpha and beta subunits stacked against one and other
polar, alpha at one end beta at the other, thus the entire microtubule is somewhat polar,
beta end is the positive end
alpha is negative end
52
what makes up actin filaments
2 strands of intertwined actin, helical
| 7nm
53
differences in the proteins constituting intermediate filaments
centers of the proteins making up these are identical
heads and tails are different are in 4 classes
1-keratin filaments in epithelial cells- most diverse class
2-vimentin fimaments in connective/muscle/supporting nervous tissue
3-neurofilaments
4nuclear fimalments- found in nuclear lamina of all cells
54
defects in intermediate filaments
1-epidermolysis bullosa simplex where keratin genes stop formation of keratin filaments, skin is very vulnerable
2-Lou Gehrigs disease where accumulation of neurofilaments in cellbodies occurs
3-progeria where defects in nuclear lamina causes people to age prematurely
55
nuclear lamina vs plasma membrane intermediate filaments
plasma membrane- steel cable like structure of joined proteins
nuclear lamina- thin 2D meshwork of proteins called lamins
56
Nuclear Lamina Intermediate filaments during proliferation
During proliferation, the lamina disassembles during mitosis, then reforms once fully divided
this process is controled by phosphorylation & dephosphorylation of the lamins
when phosphorylated, the lamins weaken and fall apart
when dephosphorylated the lamins gain strength and regain their composure
57
further stabilization of intermediate filaments occurs by what
intermedate filaments are further stabilizaed by accessory proteins like plectin which cross link filaments into bundles, connected them to microtubules and actin filaments.
58
centrosome
where microtubules grow out of
fixed to the nucleus
sphere with small nucleating sites (gamma tubulin) where microtubules grow out of
the microtubules grow out from the sphere,and can around the nucleus
centrioles are inside
59
why do microtubules need centrosomes to be created
its very hard to create microtubules from scratch, much more efficient to start from a precreated start from centrosomes
can control more precisley where they form as well
60
dynamic instability
ability of microtubules to grow and shrink instantly, switching back and forth until they disappear or they reach their destination
61
dynamic instability and GTP hydrolysis
tubulin dimers hydrolize GTP
each tubulin dimer has one GTP which goes to GDP after it joins the microtubule
this can happen so fast that dimers can still contain GTP in the microtubule-these pack together and are strong
62
colchicine/vinblastin
binds to free dimers and prevents them from aggregating into microtubules
eventually all microtubules disappear
stops cell from dividing
eventually dies
63
taxol
binds to microtubules and prevents them from losing subunits
making microtubules grow but not shrink
stops cells from dividing
eventually dies
64
why do cells modify dynamic instability
they modify it during reproduction
different specialized cells need different levels of microtubule growth
polarized cell
65
ability of molecules to be transported by diffusion and microtubule transport
10cm a day - microtubule transport
| years if ever- diffusion
66
how to microtubules participate in cell polarization
microtubules act as a link between positive and negatives ends
it transports proteins to which end they would like to go to which adds to the polarization
67
kinesins
motor protein that moves cargo towards outside/positive end
| looks like a twisted nutsack
68
dyneins
motor protein that moves cargo towards the inside/negative end
looks like it has thick thighs
69
how does one use flouresent marker proteins to view motor protiens
scientists attach a flourecent marker to the motor protein and can then watch it "walk" along microtubules
70
functions/movement differences in flagella and cillia
cillia-hairlike structures 25nm a lot on one cell, move like a whip moves fluid across cell
flagella-moves the cell larger,
71
arrangement of microtubules in cillia/flagella
in a ringlike fashion around the center
| hled together by dynein arms and linking proteins
72
cilliary dynine helps make waves with flagella/cillia how
the sliding force between the icrotubules is converted to a bending motion everything together in the ringlike structure helps 'whip' the cillia
73
cell structures made by actin
microvilli, contractile bundles in muscle, move the cell by contractions, phagocytosis stuff
74
microtubules vs actin filaments
microtubules-hollow, made up of dimers
actin filaments- two lines twisted around each other much smaller 7nm
rarly in isolation all crosslinked
both have a plus and minus end
75
how do actin grow
grows by addition of monomers, rate of growth is very fast at plus than at minus end
unstable by itself
76
what is treadmilling
replacing links in the actin filament by adding monomers at the plus end which replaces one at the minus end
77
cytochalasin and latrunculin
prevents polymerization of actin
78
phalloidin
stabilizes actin against depolymerization
79
thymosin/profilin
keeps actin in cells from polymerizing totally into filaments by binding to monomers
keeps actin in reserve until required
80
cell cortex structure/function
actin filament rich cytoplasm beneath plasma membrane
| creates movement/contraction
81
lamellipodia
helps the cell move
| meshwork of actin, protrudes towards plasma membrane
82
filopodia
at leading edge of surface advancing tip of cell
| thin stiff protursions
83
process of moving cell
the actin filaments (lamellipodia and filopodia) push out the membrane without tearing it in one direction
once touching down on a good surface they stick using integrins they then contract the other side
84
ARP & formins
actin related proteins works with lamelipodia
these bind to actin near where it wants to move then actin monomers bind to it and create actin filaments to move the cell in one direction
formins works with filopodia
these attach to actin and actin monomers bind to it in a straight line in the direction it wants to go
85
Rho
monomeric GTPase
| can promote activity of ARPs formins and can promote crawling
86
myosin 1
binds to and hydrolyzes ATP which makes energy for movement along actin towards plus end
CARRIES CARGO like vesicles or proteins
present in all cell types
head and tail, head binds to actin which hydrolyzes ATP allowing it to move up actin
the tail varies it determines the cargo it carries
87
myosin 2
a dimer, made of 2 ATPases
head end with 2 heads, tail end is two coils
can come together with other myosin 2s to create a myosin filament
used in muscles to contract
88
skeletal muscle fiber
large multinucleated cells formed by the fusion of smaller cells
cytoplasm is made up of myofibrils
looks like a giant cylinder that when cut open is full of myofibrils
has nucleases scattered over it
89
myofibrils
what makes up skeletal muscle fibers cytoplasm
contractile part of muscle cell
made of chain of small contractile units called sarcomeres that are 2.5um
90
sarcomeres
the small units that make up myofibrils and skeletal muscle fibers
the actual myosin filaments actin filaments and Z discs
the molecular level where muscles contract and relax
91
ATP in muscle contractions
1) the myosin filaments are bound to ADP and a phosphate
2) the phosphate leaves the myosin filament and the head binds to the actin which the head the binds to and pushes down
3) ADP leaves the head of the myosin and ATP replaces it pushing the myosin head back into a 'cocked' position
4) the ATP is hydrolized into an ADP and a phosphate and the cycle repeats
92
how does excitation of the muscle cell raise calcium concentrations in the cell
the AP is transferred into the muscle cell into t tubules which transfer the AP all across the cell
when the AP hits the cell, Ca ions are released by the ER releasing them into the cell
93
how do calcium ions make a muscle contract
troponin and tropomyosin are bound to actin, in this state muscles cant contract
when calcium ions flood the cell, these both fall off the actin and the myosin can contract
94
how do calcium ions contract non voluntary muscles
calcium ions flood the cell
a kinase activates phosphorylation of myosin and an ATPase
these in conjunction allow the myosin to bind to actin which allows for contractions
