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BIO 2600 > Chapter 16 > Flashcards

Chapter 16 Flashcards

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1
Q

signal transduction

A

converting a signal from one form to another

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2
Q

endocrine signal and example

A

long-lived ligands (hormones) that travel through the circulatory system to induce changes in distant target cells
- insulin released by B-cells of pancreas

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3
Q

paracrine signaling

A

short-lived ligands (growth factors) that affect nearby target cells (local)
secrete to ECM
wound healing, regulating inflammation at infection sites

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4
Q

autocrine signaling

A

paracrine signals where cells respond to their own signals that they secrete
- T cells (macrophages) with IL-6 secretion
- common in diseases, cancer cells/angiogenesis

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5
Q

neuronal signaling

A

release of short-lived ligands (neurotransmitters) into synapse

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6
Q

contact signaling

A

membrane bound signaling molecule binds to receptor on another cell
- important in development and differentiation

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7
Q

notch signaling

A

contact signaling where delta signal protein attaches to notch (delta receptor) on target cell
- Notch is a transcription regulator that cleaves its tail when bound to delta signal
-C-term tail enters nucleus to regulate transcription

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8
Q

lateral inhibition in development of fruit flies

A

single cell in a sheet of epithelial cells differentiates to become a nerve cell
-its delta signal protein attaches to notch on surrounding epithelial cells and inhibits them from differentiating

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9
Q

cell surface receptors

A

bind to large/hydrophilic ligands that cannot pass through PM

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10
Q

intracellular receptors

A

bind to small/hydrophobic ligands that can pass through the PM

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11
Q

factors that influence how different cells respond to the same signal/ligand

A

expression of certain receptors
intracellular relay system
intracellular targets
(same signal has different effects on different cell types)

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12
Q

“tailoring” of a cell response

A

thousands of different receptors allow cells to respond to different COMBINATIONS of those signals

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13
Q

fast cellular signal response

A

signal affects the activity of existing proteins
- skeletal muscles contract within ms because it opens existing ion gated channels

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14
Q

slow cellular signal response

A

response that requires gene triggering is slower (mins to hours)
- cell growth/ division

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15
Q

small hydrophobic hormones

A

steroids (testosterone, estradiol, cortisol) secreted by adrenal cortex, testes, ovaries
- derived from cholesterol
- bind to nuclear receptor superfamily of transcription regulators

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16
Q

thyroxine

A

thyroid hormone
secreted by thyroid gland
derived from tyrosine
stimulates metabolism in many cells

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17
Q

cortisol

A

hormone released by adrenal gland in starvation, stress, exercise
-signals the liver to increase glucose production from amino acids (upregulation of gluconeogenesis genes)

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18
Q

effector proteins

A

target of intracellular signaling molecules; change behavior of cells in various ways

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19
Q

functions of molecules in signaling cascade

A

relay, amplify, integrate, distribute, feedback

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20
Q

signal integration

A

cell can receive signal from more than one intracellular pathway and integrate them before moving signal onward

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21
Q

signal distribution

A

signals can be distributed to more than one signaling pathway or effector protein

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22
Q

feedback regulation of a signal

A

process in which late product of the pathway inhibits or activates an enzyme acting early in the pathway

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23
Q

two classes of molecular switches

A
  • activated/inactivated by phosphorylation
  • binding GTP (active) and GDP (inactive)
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24
Q

regulation of phosphorylation (enzymes)

A

kinases (phosphorylate): serine/threonine kinases and tyrosine kinases
phosphatase (dephosphorylate)

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25
GEFs
Guanine Exchange Factors: activate GTP-binding proteins by promoting exchange of GDP for GTP
26
GAPs
GTPase-activating proteins: turn GTP;-binding proteins off by promoting GTP hydrolysis
27
example of ion channel coupled receptors
acetylcholine receptor in skeletal muscle cells converts chemical to electrical signal
28
action of enzyme coupled receptors
usually single-pass membrane proteins activate enzymes in response to signal or are enzymes themselves (mostly kinases)
29
examples of enzyme coupled receptors
IRE1 and PERK in UPR
30
GPCRs
G-protein coupled receptors; 7-pass transmembrane proteins that activate membrane-bound G-proteins (GTP-binding proteins) which initiates signal cascade
31
makeup of G-proteins
three subunits: alpha, beta, gamma alpha and gamma tethered to PM by lipidation alpha subunit binds GDP/GTP
32
Activation of G protein process
- Inactive G-protein is bound to GDP - signal molecule binds to GPCR, activates receptors, GDP dissociates from G-protein - GTP binds to alpha subunit - alpha dissociates from beta/gamma and both can interact with proteins to further relay signal
33
how GPCRs turn off
alpha subunit is a GTPase that will hydrolyze GTP to GDP
34
Gs vs Gi (G proteins)
stimulate vs inhibit
35
targets of G-proteins
channels or enzymes Channel coupled= fast/immediate Enzyme targets (transcription regulators) take longer; most common are adenylyl cyclase and PLC (phospholipase C)
36
coupling of GPCRs to K+ channels
-acetylcholine binds to gcprs on heart muscle cells -> gcpr activation -activated beta/gamma complex binds to K+ channel and holds in open conformation - K+ released out of cell, hyperpolarization, contraction/heartbeat slows down
37
signals that increase heartbeat
adrenaline aka epinephrine
38
cholera toxin action
modifies alpha subunit of Gs; locks G protein in active state (cannot hydrolyze GTP) -> stimulates adenylyl cyclase enzyme causing influx of Cl- and hence water into gut lumen -> extreme diarrhea and dehydration, can be fatal
39
cAMP phosphodiesterase
enzyme that converts cyclic AMP (cAMP) back to AMP - terminates signal
40
adenylyl cyclase enzyme activity
converts ATP to cAMP
41
primary messengers
ligand binding
42
second messengers
intracellular signaling molecules released by the cell; amplify and continue signal
43
glucose/cAMP relationship
glucose inhibits cAMP synthesis to maintain high ATP conditions -tells the cell more ATP doesn't need to be made
44
cAMP initiates low or high energy pathways
low energy pathways
45
caffeine effect on cAMP
caffeine inhibits caffeine breakdown- causes fast heart rate, muscle shaking
46
cascade pathway of G-proteins activating adenylyl cyclase
activated GCPR activates alpha subunit of G-protein -> activates adenylyl cyclase -> produces cAMP -> cAMp binds/activates PKA -> active PKA phosphorylates downstream targets; changes protein activity
47
PKA
protein kinase A, activated by binding of cAMP
48
epinephrine (adrenaline) effect on GCPR pathway in skeletal muscle cells
stimulates glycogen breakdown
49
cAMP causes what output signal
varies based on what proteins get phosphorylated cAMP induces PKA-dependant protein phosphorylation - can regulate transcription factor activity
50
epinephrine (adrenaline) effect on GCPR pathway in heart cells
increase heart rate
51
epinephrine (adrenaline) effect on GCPR pathway in fat cells
breakdown of fats to fatty acids
52
adrenergic receptors
receptors that bind adrenaline/epinephrine
53
adrenaline GCPR full pathway
adrenaline -> GPCR activate -> G-protein activates -> adenyl cyclase activates -> cAMP production -> activates PKA -> 1. increase heart rate 2. breakdown of glycogen in skeletal muscles 3. breakdown fats to fatty acids Response prepares body for SUDDEN ACTION
54
result of mutation that constitutively activates PKA in skeletal muscle cells
decrease in the amount of glycogen available since glycogen phosphorylase would always be activated
55
PLC
enzyme that cleaves inositol phospholipids to inositol triphosphate (IP3) and diacylglycerol (DAG) bound to the cytosolic side of PM
56
result of IP3 released to cytosol
binds to Ca2+ channels at the ER, Ca spills into cytosol and has many effects as second messenger (actin/myosin contraction, neurotransmitter release)
57
calmodulin
Ca2+ binding protein (4 sites) activates Ca2+/calmodulin dependent protein kinases (CaM-kinases)
58
CaM kinases activity
phosphorylates serines and threonines of target proteins
59
GCPR/NO pathway
acetylcholine binds GCPR on epithelial cells -stimulates an increase in cytosolic Ca2+ - activates nitric oxide synthesis from Arg - NO diffuses to neighboring cardiac muscle cells - NO binds guanylyl cyclase which converts GTP to cGMP -causes smooth muscle cells to relax REDUCES BLOOD PRESSURE
60
examples of primary messengers
insulin, adrenalin, acetylcholine
61
examples of second messengers
Ca2+, cAMP, Ap3, DAG
62
RTKs
Receptor Tyrosine Kinases common single-pass enzyme coupled receptors spanning PM -binding of signal molecule causes them to dimerize (to associate together)
63
dimerization of RTKs
activates kinase domains (phosphorylate each other on specific tyrosine) -autophosphorylation
64
SH2 domain
domain on target domain that binds to phosphorylated tyrosine (docking site for SH2) on RTK
65
How is RTK signal turned off
-Tyr phosphatase removes phosphate - Entire receptor can be recycles
66
Ras
small GTP binding protein that acts as a second messenger -anchored to cytosolic face of PM by lipidation -found mutated in 30% of cancers-constitutively active Ras (oncogene)
67
activation of Ras by RTK
activated RTK recruits Ras-GEF (via adaptor protein) to activate Ras -> onward signal transmission
68
Ras amplification cascade
Phosphorylation cascade of serine/threonine kinases (via ATP hydrolysis) Ras activates MAP 3K -> activates MAP KK -> activates MAP kinase -> changes in protein activity and gene regulation
69
advantage of 3 kinase pathway
allows for signal integration
70
PI-3-Kinase-Akt Pathway
phosphoinositide 3-kinase (activated, bound to P-RTK) phosphorylates inositol phospholipid -> recruits serine/threonine protein kinase Akt (protein kinase B)
71
Akt activation
recruited to P-inositol phospholipid, activated by protein kinases 1 and 2 (which phosphorylate Akt) activated by different pathways (integration)
72
activation of Akt direct effects
Akt released from PM Akt phosphorylates Bad (inactivates) Bad releases active Bcl2 Active Bcl2 inhibits apoptosis
73
Unphosphorylated Bad state
promotes cell death (apoptosis) by inhibiting Bcl2 (which suppresses apoptosis)
74
activation of Akt indirect effects
activated Akt indirectly activates TOR (serine threonine kinase) by phosphorylating and inhibiting TOR suppressor -caused by binding of extracellular growth factors to RTK receptor
75
TOR
target of rapamycin active = cell growth inactive = autophagy
76
rapamycin
inhibits TOR, promotes autophagy anticancer
77
how to determine binding sites of RTKs and target protein of specific P-Tyr
mutant receptors -replace tyrosine with amino acid that won't bind target protein (Phe)
78
introducing a constitutively active Ras rescues a mutation in protein X, but not Y . . . which is upstream of Ras and which is downstream
X is upstream of Ras (activated Ras can recover the signal) Y is downstream (active Ras cannot recover signal)

BIO 2600 (15 decks)

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