Exam 2 Flashcards
(314 cards)
1
Q
How do phospholipids influence cell membranes
A
impact what molecules can pass through
permeable to uncharged, nonpolar, & small polar molecules
2
Q
How does cholesterol influence cell membranes
A
membrane packs tightly
allows protein to cluster into functional groups
3
Q
Diffusion barriers of cholesterol enable what
A
apical-basolateral cell polarization
4
Q
How do glycolipids influence cell membranes
A
maintained on extracellular leaflet
asymmetry
5
Q
How does phosphatidyl serine influence cell membranes
A
maintained on intracellular leaflet
asymmetry
6
Q
What does phosphatidyl serine signal if on he outer leaflet
A
phagocytosis
7
Q
What are the two types of transporters
A
active or passive
8
Q
Are transporters fast
A
no, involve a conformation change
9
Q
What are channels
A
small holes in membrane
10
Q
Are channels fast
A
yes, do not involve a conformation change
11
Q
Are channels often selective
A
yes
12
Q
Do channels require energy or a conformational change
A
no
13
Q
What are non-gated ion channels (ex?)
A
channels that are always open
K+ leak channels
14
Q
What are voltage-gated ion channels (ex?)
A
channels that are “gated” electrically
K+ or Na+ voltage-gated channels
15
Q
Sensors of voltage-gated channels respond to what
A
changing charge on plasma membrane
16
Q
What are ligand-gated ion channels (ex?)
A
channels that are “gated” and require ligands to bind to open
Na+ ligand-gated channels
17
Q
Describe the chemical gradient
A
ions concentration difference b/w the inside & outside of the cell
18
Q
Describe the electrical gradient
A
electrical difference b/w the inside & outside of the cell
19
Q
What is the electrochemical gradient
A
takes into account both the electrical & chemical gradients of ions
20
Q
What molecules receive a greater pull to enter into the cell (not considering concentration gradient)
A
positive ions
cell interior is negative
21
Q
Why is the interior of the cell negative
A
large, negatively charged organic (protein) molecules are on the inside of the cell & cannot leave
22
Q
Membrane potential depends on what
A
K+ leak channels & Na+/K+ pump
23
Q
What is membrane potential expressed as
A
voltage
24
Q
What has to be known in order to calculate membrane potential
A
permeability of membrane to ions & presence of open channels
25
What factors determine resting membrane potential inside the cell
negatively charged, Na+ low, & K+ high
26
At rest, what channels are open and what channels are closed
Na+ closed
| K+ leak channels open
27
Define action potential
depolarization of membrane potential
28
What are the steps of action potential
1) stimulus triggers NT ligand to open up the ligand-gated Na channel
2) Na+ starts entering cell, increasing pos charge on the inside
3) increase in pos charge on the inside opens up the voltage-gated Na+ channels to open
4) Na+ rushes in, depolarizing cell
5) secondary gated channels blocks Na+ at a certain concentration
6) depolarization triggers K+ gated channels to open
7) K+ rushes in & balances charges until blocked at a certain concentration
8) Na+/K+ pump returns membrane to its resting potential
29
Describe hyperkalemia
increase in extracellular K+
30
Does hyperkalemia result in more or less driving force inward
more
| due to electrochemical gradient
31
Would hyperkalemia increase or decrease resting membrane potential
decrease
| become less neg/ closer to 0
32
How does hyperkalemia impact action potential
closer to threshold
| more likely to happen
33
Describe hyponatremia
decrease in extracellular Na+
34
Does hypernatremia result in more or less driving force inward
less
| due to electrochemical gradient
35
Would hypernatremia increase or decrease resting membrane potential
no effect
| Na+ channels are closed at rest
36
How does hyponatremia impact action potential
makes it smaller
| shorter peak
37
What is a common cause of hyponatremia
water intoxication
38
How does hyponatremia as a result of water intoxication occur
Na+ ions diluted
water rushes into cell
edema occurs
39
Where is glycocalyx found
attached to extracellular portion of membrane proteins
40
What is glycocalyx often called
membrane decor b/c it is on the extracellular surface of cells
41
What are the compositions of glycocalyx
glycolipds & glycoproteins
42
Where do glycolipids get their diversity from
AA sequence of protein & monosaccharide combos in the polysaccharide
43
Glyco means what
polysaccharide
44
What are the functions of glycocalyx
```
immune recognition (self vs non-self)
protective barrier against bacterial invasion
pathogen receptor (viral receptor specificity)
```
45
O antigen has what
no additional glycocalyx
46
B antigen has what
added galactose
47
A antigen has what
added N-acetylgalactosamine
48
What does glycocalyx do on the intestinal epithelium
increases surface area of microvilli
| decreases # of invading pathogens
49
What cells in the intestinal epithelium have less glycocalyx
antigen sampling cells
50
Why do the antigen sampling cells have less glycocalyx
provides access to the luminal contents to sample antigens
51
Are the antigen sampling cells more or less susceptible to bacterial infection
more
52
Influenza virus hemagglutinin binds to what on epithelial cells
glycoproteins w/ sialic acids
53
Different sialic linkages result in different binding & impacts what
where the virus infection is permissible
54
H1N1 hemagglutinin subtype 1 binds to what
alpha 2-6 linked sialic acids
55
Where is alpha 2-6 linked sialic acids found
upper respiratory tract
| so this is where H1N1 infects
56
H5N1 hemagglutinin subtype 5 binds to what
alpha 2-3 linked siliac acids
57
Where is alpha 2-3 siliac acids found
avian intestinal mucosa
in humans, lower respiratory tract
so this is where H5N1 infects
58
What part of SARS-CoV-2 is heavily glycoxylated
spike protein
59
The glycan shield of SARS-CoV-2 limits what
potential antibody binding sites
60
What are the components of ECM
fibroblasts, ground substance, & collagen
61
What do fibroblasts do
make collagen & ground substance
62
What is found in ground substance
proteins
63
What does collagen provide
tensile strength
64
What are glycosaminoglycans
GAGs
| large, highly neg charged polysaccharides
65
What are GAGs called when attached to a protein core
proteoglycans
66
What GAG is not attached to a protein core
hyaluronic acid
67
What is the function of hyaluronic acid
pulls in H2O
plumps up skin & resists compression
lubricant in joint fluid
68
GAGs represent < 10% of entire ECM, but they do what
occupy most of the space
69
How do GAGs provide compressive strength
form hydrated gels
70
What causes GAGs to swell
neg charge attracts cations
| cations pull water in
71
When do GAGs help with cell migration
during development & repair
72
In certain tissues, GAGs have what function
filtration
73
GAGs serve as what for other molecules
binding sites
74
GAGs act as attachment to what
fibrous elements
75
Do GAGs or glycoproteins branch
glycoproteins
76
Do GAGs or glycoproteins have repeating units
glycoproteins
77
Why do GAGs fill the ECM
bend, but cannot fold tightly as a hydrogel
78
Is collagen the same everywhere
no, different types in different tissues
79
Collagen is synthesized where
in the cell
80
Is collagen constitutively expressed
yes
81
What does collagen require to mature
extracellular proteolytic processing
82
Collagen arrangement defines what
tissue strength properties
83
Strength based on collagen can be what
in many directions or one direction
84
Shar pei skin (slimy-ness) is the result of what
overproduction of hyaluronic acid
85
What direction is skin strong in
many directions
86
What direction are tendons strong in
one direction
87
AA sequence of the glycoprotein can be different how
diverse attachment site of protein sequence
88
Monosacharide combinations in the polysaccharide portion of glycoprotein can be different how
permutations in monosaccharide order
| branch points add additional complexity
89
Besides GAGs and fibers, what is the other component of ECM in CT
non-collagen glycoproteins
90
Ehlers-Danlos syndrome is a result of what mutation
ADAMTS2 protease
91
ADAMTS2 protease does what
converts pro-collagen to collagen
92
Ehler-Danlos syndrome causes a defect in collage synthesis called
Cutis Hyperelastica
93
How does Cutis Hyperelastica come about
C-terminus of pro-collagen is cut off, but the N-terminus is not removed
94
What is the functional result of the N-terminus being removed
skin has reduced tensile strength
| increased stretch
95
Elastic fibers are a network of
elastin molecules
96
Elastic fibers are abundant where
aorta, ligaments, & zonular fibers of the eye
97
What scaffold helps elastic fibers form myofibrils
fibrillin
98
What species does Marfan Syndrome occur in
cattle & humans
99
What caused Marfan Syndrome
mutation in fibrillin
100
What type of mutation is Marfan Syndrome
autosomal dominant
101
Marfan Syndrome results in what
dysfunction in elastic fibers
102
Those w/ Marfan Syndrome are at risk of what
aortic aneurism
103
What does the first messenger in cellular signaling do
receive extracellular signal
104
What does the receptor/transducer in cellular signaling do
transmits signals across plasma membrane (protein)
105
What does the primary effector in cellular signaling do
binds to proteins & regulate their activity
106
What does the secondary messenger & secondary effector do in cellular signalin
pass along the signal
107
What are primary & secondary effectors
proteins or enzymes
108
What are secondary messengers
small molecules
109
What are the two types of molecular switches
phosphorylation & GTP binding
110
What does protein kinase do
use ATP to phosphorylate a protein
111
Do protein kinases (typically) activate or inhibit proteins
activate
112
What does protein phosphatase do
removes phosphates from proteins
113
Do protein phosphatases (typically) activate or inhibit proteins
inhibit
114
How are molecules activated that use GTP binding
GTP replaces the GDP bound to the protein
115
How are molecules inactivated that use GTP binding
phosphate is removed through GTP hydrolysis
116
What molecules remove GDP so free GTP can bind (activate)
GEFs
117
What molecules convert GTP -> GDP (inactivate)
GAPs
118
Signal ____ on activation and signal _____ before being inactivated
in, out
119
Transmitter gated membrane receptors is a type of what
cell surface receptor
120
How are transmitter gated membrane receptors activated
ligand (signal molecule) binds to a receptor
| channel opens for ions to flow through
121
What is an example of a Transmitter gated membrane receptor
acetylcholine receptor at neuromuscular junctions
122
Different G-protein coupled receptors (GPCRs) can be activated by the same signal but do what
produce different responses depending on the cells
123
GPCRs are important as what
drug targets
124
GPCRs activate what
alpha subunit of trimeric G-proteins
125
How do GPCRs activate the alpha subunit of trimeric G-proteins
GDP/GTP acivity switch
126
What are the parts of a trimeric G-protein
alpha, beta, & gamma
127
What do trimeric G-proteins allow GPCRs to do
become coupled to downstream activities
128
H1 histamine receptor is a type of what
GPCR
129
What does the alpha unit of the trimeric G -protein activate, following histamine binding to the H1 histamine receptor
phospholipase C
130
Phospholipase C cleaves what
PIP2 into IP3 & DAG
131
IP3 activates what
Ca2+ release from ER
132
DAG & Ca2+ activate what
protein kinase C
133
protein kinase C activates what
NF-kbeta
134
NF-kbeta causes what
inflammation & hives
135
Receptor Tyrosine Kinase (RTK) is a type of what
enzyme-linked receptor
136
What binds a signal molecule for RTKs
extracellular domain
137
What leads to activation of RTKs
dimerization
| allows for phosphate binding
138
What are recruited to activated RTKs to pass the signal along
relays
139
What generatd many binding sites on the RTK for signaling proteins
trans-autophosphorylation after dimerization
140
Ras has what type of activity switch
GDP/GTP
141
A mitogen signal for cell division activates what
RTK
142
What activates Ras GEF
adaptor protein bound to RTK
143
What does Ras GEF do
removes GDP from Ras protein
144
Activated Ras initiates what sequence of events
Mitogen-activated protein kinase (MAPK) cascade
145
Each step of MAPKKK -> MAPKK -> MAPK involves what
ATP hydrolysis
146
After the MAP's, what happens & what does it lead to
change in protein activity & gene expression
| leads to cell division
147
Where do pattern recognition receptors (PRRs) operate
on cell surface & extracellularly
148
What do PRRs function as
act as pathogen sensors
149
PRRs recognize what
Pathogen-associated molecular patterns (PAMPs)
150
PAMPs consist of what
double-stranded RNA (viruses) or lipolysaccharides (bacteria)
151
PRRs create a signal to activate what
an innate immune response
152
What are examples of PRRs
*Toll-like receptors (TLRs)*
NOD-like receptors (NLRs)
C-type lectin receptors (CLRs)
RIG-I-like recpetors (RLRs)
153
PAMP binds to a TLR receptor & the adaptor proteins activate
IKK complex
154
IKK complex does what
phosphorylates IKB
155
When IKB is phosphorylated, what happens
gets degraded in proteosomes
156
Active IKB functions to do what
inhibit NF-kbeta
157
Active NF-kbeta does what & causes what (different answer than hives one)
alters gene expression; innate immune response
158
Cytokine binding to cytokine receptors causes what
dimerization
159
Dimerization of cytokine receptors results in
activation of JAK kinase
160
Phosphorylation of JAK kinase does what
recruits STAT proteins
161
Phosphorylated STATs do what
dimerize & translocate to nucleus to alter gene expression
162
What is the source of somatotropin (GH) & how is it transported through the body
anterior pituitary
| thus, GH sent through cardiovascular system
163
What are the target tissues for GH
skeletal muscle, adipose tissue, bone, & liver
164
MAP kinase cascade causes what type of growth effects
direct & systemic
165
MAP kinase cascade involves Ras signalling that leads to the transcription & translation of factors that cause what
cell cycle entry -> proliferation
166
GH signaling w/ MAP kinase cascade involves
Ras signaling & enzyme-linked receptor (RTK)
167
GH via MAP kinase cascade stimulates what
muscle, chondrocyte (cartilage), & bone growth during childhood
168
JAK-STAT pathway for GH stimulates what
induction of IGF-1 in liver
169
Production of IGF-1 in liver promotes what
growth of liver, bone growth, protein synthesis, increased muscle mass, & activation of stored fat
170
JAK-STAT pathway involves what molecules
growth hormone
GH receptor (dimerizes)
JAK kinases
STAT proteins
171
Do Great Danes or Chiuahuas have more IGF-1
Great danes
172
Elevated GH in mice results in
gigantism
173
GH deficiency in mice results in
dwarfism
174
GH insensitivity in mice leads to
dwarfism
175
Over the long run, decreased GH signaling leads to
a longer lifespand
176
What does bovine somatotropin do
stimulate IGF-1 production -> survival of mammary alveolar cells
177
Recombinant bovine somatotropin results in what changes in the cow
increased milk production
| increased growth
178
Glycogen breakdown is stimulated in muscle by
adrenaline (epinephrine)
179
Glycogen breakdown is stimulated in the liver by
glucagon
180
What makes cAMP
adenylate cyclase (AC)
181
What breaks cAMP
PDE
182
What is protein kinase A (PKA)
dimer of dimers
183
cAMP has what effect on PKA
removes regulatory part
| allows catalytic part to be active
184
Adrenaline & glucagon are signal molecules that first activate what to lead to glycogen breakdown
GPCR
185
Activation of the alpha subunit of the trimeric protein results in activation of what in glycogen breakdown
adenylate cyclase (AC)
186
AC causes the conversion of what into cAMP
ATP
187
cAMP activates PKA, resulting in
glycogen -> glucose 1-phosphate
188
If GH hormone releasing hormone stimulates a similar cascade to glycogen breakdown, what does PKA activate instead
CREB
189
Activated/phosphorylated CREB does what
results in gene transcription of GH
190
What is the source of adrenaline
adrenal medulla
191
What are the physiological effects of adrenaline
increased heart rate
increased resp rate
pupil dilation
glycogen breakdwon
192
alpha 1 activates what, leading to what intracellular signaling events
phospholipase C
leads to PIP3 -> IP3 + DAG
Ca2+ release
193
Ca2+ release as a result of alpha 1 causes what
smooth muscle contraction of GI & peripheral blood vessels
194
alpha 2 does what, leading to what
represses AC
| decreased levels of cAMP
195
Decreased cAMP as a result of alpha 2 causes what
smooth muscle contraction of GI sphincter
196
beta does what, leading to what
activates AC
| increased levels of cAMP
197
Increased cAMP as a result of beta causes what
heart muscle contraction (increases heart rate), smooth muscle relaxation, glycogenolysis, & opening of bronchioles
198
What kind of molecule is caffeine
xanthine alkaloid
199
What is the source of caffeine
leaves, seeds, & fruits of some plants
200
What are the physiological effect of caffeine
neurostimulant
| increased heart rate
201
How does caffeine act as a neurostimulant
counteracts inhibitory effect of adenosine
202
How does caffeine increase heart rate
PDE inhibited
cAMP conc increases
PKA activity increases
203
What is the source of cholera toxin
vibrio cholerae
204
What are the physiological effects of cholera toxin
efflux of ions & water into small intestine
205
What molecules does cholera toxin affect
alpha subunit of GPCR
206
What effect does cholera toxin have on the alpha subunit of GPCR
permanently activates it
207
How does cholera toxin permanently activate the alpha subunit of GPCR
catalyzes a covalent modifcation
| ADP-ribose from NAD+ locks onto an Arginine side chain
208
When the alpha subunit is permanently activated by the cholera toxin, what occurs
AC stimulated
levels of cAMP & PKA increase
chloride channels open
209
What is a drug that represses AC
enkephalin
210
What are the phases of the cell cycle
G1, S, G2, & M
| G0
211
G1 phase involves
cell growth
| copy of organelles
212
S phase involves
DNA synthesis
| chromosome replication
213
G2 phase involves
cell growth
| synthesis of proteins/ organelles
214
M phase involves
mitosis
| chromosomes separated
215
G0 phase involves
cell cycle arrested
216
Cyclins do what
activate CdK
217
Cyclins allow for control during the cell cycle b/c they undergo
synthesis & degradation
218
What are examples of the different types of cyclins
G1/S cyclin
M cyclin
S cyclin
219
What does CdK stand for
cyclin-dependent kinase
220
When are CdKs active
only when their cyclin activator is present
221
What do CdKs do
phosphorylate other molecules to activate them
222
Is CdK expression constant
yes
223
Activity of CdK rises & falls corresponding to
cyclin binding
224
What is CAK
CdK activating kinase
225
Cyclins cause CdK to undergo a conformation change, which allows what to happen
CAK phosphorylates CdK (on threonine)
226
Do cells in G0 have a lot or a little of CAK
little
227
Wee1 kinase does what
phosphorylates active (phosphorylated) CdK to temporarily inactivate it
228
What does Wee1 kinase allow to happen
cell to grow during G2
229
Wee1 mutants are what
small
230
Cdc25 phosphatase does what
removes the inactivating phosphate to activate CdK
231
CKI stands for
cyclin dependent kinase inhibitor
232
Two types of CKI
p21 & p27
233
CKI (p21 & p27) do what
bind to the cyclin-CdK complex to inactivate it
234
When are CKIs expressed
during G0 to prevent cell cycle entry
235
What does E3 ligase SCF do
degrades inhibitor p27
| makes cyclin-CdK complex active again
236
What events does E2F activation lead to
S-phase gene transcription -> G1/S cyclin -> activated S-CdK -> S phase
237
What does Rb do when active
inactivates E2F
| prevents transcription of S-cyclin
238
Rb arrests cells at what checkpoint
G1/S
239
What does Ras do after it receives a mitogen signal
indirectly inactivates Rb
240
What events happen when Rb is inactivated
EF is liberated
cells pass through the G1/S checkpoint
cell division occurs
241
What events lead to the indirect activation of Rb by Ras
MAP kinase cascade
activation of G1 cyclin transcription
G1 & cyclin-dependent kinase activation
G1-CdK dependent phosphorylation of Rb
242
What does mdm2 (E3 ligase) do
binds & inactivates p53
243
What does mdm2 promote
protease degradation of p53
244
p53 leads to what cellular events
cell cycle arrest, DNA repair, & cell cycle restart
| apoptosis
245
p53 promotes what
cellular & genetic stability
246
p53 is active at what checkpoint
G2/M
247
DNA damage leads to the activation of p53 by
phosphorylation
248
Activated p53 binds to the regulatory region of what
p21 gene
249
After p53 binding, translated p21 does what
inactivates G1/S-CdK & S-CdK complexes
250
The inactivation of the G1/S-CdK & S-CdK complexes leads to
cell cycle arrest & DNA repair
251
What is the G1/S checkpoint
start transition
| restriction point
252
In the G1/S checkpoint, the cell checks on what
cellsize
nutrients
growth factors
DNA damage
253
After the G1/S checkpoint, what happens
enter S phase or G0
254
What is the G2/M checkpoint
gap to mitosis transition
255
In the G2/M checkpoint, the cell checks on what
DNA damage
| DNA replication
256
After the G2/M checkpoint, what can happen
enter M phase
pause to repair damage
undergo apoptosis
257
What is the M/G1 checkpoint
metaphase-to-anaphase transition
258
In the M/G1 checkpoint, the cell checks on what
chromosome attachment
259
Non-functional Rb leads to what
no break before S phase
| aggressive cancer
260
Hyperactive Ras (meaning Ras activates too early) promotes what
activation of MAP-kinase cascade
cells divide inappropriately b/c Rb is inactivated
aggressive cancer
261
p53 mutations in the DNA binding domain make it unable to promote transcription of p21, so what happens
inability to inactivate G1/S-CdK & S-CdK complexes
cell progresses right into S phase
aggressive cancer
262
Apoptosis is described as what type of process
controlled developmental process
263
Apoptosis is considered what type of pathway for cells if they are not provided with what type of factors
default, survival
264
Apoptosis is initiated by
viruses
organ/ tissue development
DNA damage
265
Apoptosis promotes what
homeostasis
266
Does apoptosis involve single cells or clusters
both
267
Does apoptosis involve cell swelling or shrinkage
shrinkage
268
Does apoptosis involve controlled or random DNA fragmentation
controlled
269
Does apoptosis involve intact or broken cell membranes
intact
270
Does apoptosis release the cytoplasm through pores or bodies
apoptotic bodies
271
Does apoptosis involve inflammation
no
272
Caspase have what active site & cleave where
active site cysteine
| cleave at aspartic acid
273
What do adaptor proteins do to caspases
dimerize, activate, & cleave the initiator caspase
274
The active initator caspase does what
cleaves the executioner caspase to activate it
275
The active executioner caspase does what
cleaves multiple subunits
276
The cleavage of multiple subunits leads to what
apoptosis
277
Each cleavage results in what
conformational change
278
Cells are removed in a controlled fashion as what happens
caspases amplify their signals
279
A few activated caspases lead to
cleavage of cytosolic protein
280
Many activated caspases lead to
clavage of nuclear lamin
281
Intrinsic pathway of caspase activation is via what type of pathway
mitochondrial
282
Intrinsic pathway is activated by
intracellular factors (oxidative stress, hypoxia, nutrient deprevation, & DNA damage)
283
Intrinsic pathway results in what
mitochondrial membrane permeabilization
| cytochrome c leakage into the cytoplasm
284
What binds to cytochrome c in the cytoplasm
adaptor proteins
285
Adaptor proteins w/ cytochrome c form what
apoptosome
286
Apoptosome recruit what that forms what
caspases
| forms an active initiator caspase
287
Active iniatiator caspase does what
activates executioner caspases
288
Executioner caspases lead to
cellular breakdown
| apoptosis
289
What molecule creates pores for cytocrhome c to leak out
Bax
290
Is Bax pro-apoptotic or anti-apoptotic
pro-apoptotic
291
What does Bcl2 do
inhibits Bax
292
Is Bcl2 pro-apoptotic or anti-apoptotic
anti-apoptotic
293
What does Bad do
sequesters Bcl2
| allows Bax to create pores
294
Is Bad pro-apoptotic or anti-apoptotic
pro-apoptotic
295
What molecule promotes the aggregation of Bax so that it can create pores
p53
296
What does the extrinsic pathway for caspase activation involve
damaged cell displayes a death receptor on its surface
297
What recognizes the death receptor
killer lymphocyte
298
Cell-cell binding of the killer lymphocyte to the target cell results in
assembly of adaptor proteins into a death-inducing signaling complex
299
The death-inducing signaling complex leads to what & ultimately what
activates executioner caspases
| apoptosis
300
Cells constantly decide if they will
divide, differentiate, or die
301
Sculpting organs requires
proliferation, survival, & apoptosis
302
Inadequate apoptosis in b/w digits leads to
syndactyly
303
Too little proliferation causes
Microphthalmia - small eye phenotype
304
Microphthalmia is a result of
genetic, environmental, or infectious
| ex: maternal Vit A deficiency
305
Too much proliferation causes
```
Protein myostatin
Mighty mice
Texel sheep
Belgian blue cattle
Whippets
```
306
Protein myostatin is what
differentiation factor
| prevents myogenesis
307
Mighty mice are transgenic mice mutants with
increased muscle mass & fiber number
308
Belgian blue cattle are often called what and have a mutation in what leading to what
double muscled
mutation in myostatin
more myocytes
309
Whippets have what after a mutation in myostatin
increased muscle mass
310
Examples of second messengers
Ras, cAMP, IP3, & DAG
311
What does GH stimulate in adipose tissue
release of FAs
312
What does GH stimulate in skeletal muscle
increase nutrient uptake & utilization
313
What does GH stimulated in bone
bone growth
314
What does GH stimulate in liver
increased IGF-1
