Brainscape's Knowledge GenomeTM

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


See full index

BIO 2600 > Chapter 16 > Flashcards

Chapter 16 Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

signal transduction

A

converting a signal from one form to another

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

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

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

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

neuronal signaling

A

release of short-lived ligands (neurotransmitters) into synapse

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

contact signaling

A

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

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

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

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

cell surface receptors

A

bind to large/hydrophilic ligands that cannot pass through PM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

intracellular receptors

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

“tailoring” of a cell response

A

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

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

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

slow cellular signal response

A

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

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

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

thyroxine

A

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

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

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

effector proteins

A

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

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

functions of molecules in signaling cascade

A

relay, amplify, integrate, distribute, feedback

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

signal integration

A

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

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

signal distribution

A

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

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

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

two classes of molecular switches

A
  • activated/inactivated by phosphorylation
  • binding GTP (active) and GDP (inactive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

regulation of phosphorylation (enzymes)

A

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

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

GEFs

A

Guanine Exchange Factors: activate GTP-binding proteins by promoting exchange of GDP for GTP

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

GAPs

A

GTPase-activating proteins: turn GTP;-binding proteins off by promoting GTP hydrolysis

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

example of ion channel coupled receptors

A

acetylcholine receptor in skeletal muscle cells converts chemical to electrical signal

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

action of enzyme coupled receptors

A

usually single-pass membrane proteins activate enzymes in response to signal or are enzymes themselves (mostly kinases)

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

examples of enzyme coupled receptors

A

IRE1 and PERK in UPR

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

GPCRs

A

G-protein coupled receptors; 7-pass transmembrane proteins that activate membrane-bound G-proteins (GTP-binding proteins) which initiates signal cascade

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

makeup of G-proteins

A

three subunits: alpha, beta, gamma
alpha and gamma tethered to PM by lipidation
alpha subunit binds GDP/GTP

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

Activation of G protein process

A
  • 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
Q

how GPCRs turn off

A

alpha subunit is a GTPase that will hydrolyze GTP to GDP

34
Q

Gs vs Gi (G proteins)

A

stimulate vs inhibit

35
Q

targets of G-proteins

A

channels or enzymes
Channel coupled= fast/immediate
Enzyme targets (transcription regulators) take longer; most common are adenylyl cyclase and PLC (phospholipase C)

36
Q

coupling of GPCRs to K+ channels

A

-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
Q

signals that increase heartbeat

A

adrenaline aka epinephrine

38
Q

cholera toxin action

A

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
Q

cAMP phosphodiesterase

A

enzyme that converts cyclic AMP (cAMP) back to AMP - terminates signal

40
Q

adenylyl cyclase enzyme activity

A

converts ATP to cAMP

41
Q

primary messengers

A

ligand binding

42
Q

second messengers

A

intracellular signaling molecules released by the cell; amplify and continue signal

43
Q

glucose/cAMP relationship

A

glucose inhibits cAMP synthesis to maintain high ATP conditions
-tells the cell more ATP doesn’t need to be made

44
Q

cAMP initiates low or high energy pathways

A

low energy pathways

45
Q

caffeine effect on cAMP

A

caffeine inhibits caffeine breakdown- causes fast heart rate, muscle shaking

46
Q

cascade pathway of G-proteins activating adenylyl cyclase

A

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
Q

PKA

A

protein kinase A, activated by binding of cAMP

48
Q

epinephrine (adrenaline) effect on GCPR pathway in skeletal muscle cells

A

stimulates glycogen breakdown

49
Q

cAMP causes what output signal

A

varies based on what proteins get phosphorylated
cAMP induces PKA-dependant protein phosphorylation
- can regulate transcription factor activity

50
Q

epinephrine (adrenaline) effect on GCPR pathway in heart cells

A

increase heart rate

51
Q

epinephrine (adrenaline) effect on GCPR pathway in fat cells

A

breakdown of fats to fatty acids

52
Q

adrenergic receptors

A

receptors that bind adrenaline/epinephrine

53
Q

adrenaline GCPR full pathway

A

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
Q

result of mutation that constitutively activates PKA in skeletal muscle cells

A

decrease in the amount of glycogen available since glycogen phosphorylase would always be activated

55
Q

PLC

A

enzyme that cleaves inositol phospholipids to inositol triphosphate (IP3) and diacylglycerol (DAG)
bound to the cytosolic side of PM

56
Q

result of IP3 released to cytosol

A

binds to Ca2+ channels at the ER, Ca spills into cytosol and has many effects as second messenger (actin/myosin contraction, neurotransmitter release)

57
Q

calmodulin

A

Ca2+ binding protein (4 sites)
activates Ca2+/calmodulin dependent protein kinases (CaM-kinases)

58
Q

CaM kinases activity

A

phosphorylates serines and threonines of target proteins

59
Q

GCPR/NO pathway

A

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
Q

examples of primary messengers

A

insulin, adrenalin, acetylcholine

61
Q

examples of second messengers

A

Ca2+, cAMP, Ap3, DAG

62
Q

RTKs

A

Receptor Tyrosine Kinases
common single-pass enzyme coupled receptors spanning PM
-binding of signal molecule causes them to dimerize (to associate together)

63
Q

dimerization of RTKs

A

activates kinase domains (phosphorylate each other on specific tyrosine) -autophosphorylation

64
Q

SH2 domain

A

domain on target domain that binds to phosphorylated tyrosine (docking site for SH2) on RTK

65
Q

How is RTK signal turned off

A

-Tyr phosphatase removes phosphate
- Entire receptor can be recycles

66
Q

Ras

A

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
Q

activation of Ras by RTK

A

activated RTK recruits Ras-GEF (via adaptor protein) to activate Ras -> onward signal transmission

68
Q

Ras amplification cascade

A

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
Q

advantage of 3 kinase pathway

A

allows for signal integration

70
Q

PI-3-Kinase-Akt Pathway

A

phosphoinositide 3-kinase (activated, bound to P-RTK) phosphorylates inositol phospholipid -> recruits serine/threonine protein kinase Akt (protein kinase B)

71
Q

Akt activation

A

recruited to P-inositol phospholipid, activated by protein kinases 1 and 2 (which phosphorylate Akt)
activated by different pathways (integration)

72
Q

activation of Akt direct effects

A

Akt released from PM
Akt phosphorylates Bad (inactivates)
Bad releases active Bcl2
Active Bcl2 inhibits apoptosis

73
Q

Unphosphorylated Bad state

A

promotes cell death (apoptosis) by inhibiting Bcl2 (which suppresses apoptosis)

74
Q

activation of Akt indirect effects

A

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
Q

TOR

A

target of rapamycin
active = cell growth
inactive = autophagy

76
Q

rapamycin

A

inhibits TOR, promotes autophagy
anticancer

77
Q

how to determine binding sites of RTKs and target protein of specific P-Tyr

A

mutant receptors -replace tyrosine with amino acid that won’t bind target protein (Phe)

78
Q

introducing a constitutively active Ras rescues a mutation in protein X, but not Y . . . which is upstream of Ras and which is downstream

A

X is upstream of Ras (activated Ras can recover the signal)
Y is downstream (active Ras cannot recover signal)

BIO 2600 (15 decks)

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