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CELL 302 > Lecture A3 > Flashcards

Lecture A3 Flashcards

1
Q

To properly establish cell fate and diversity, cells need to do what?

A

properly communicate

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2
Q

Cell diversity in the human body is driven by two events: ______

A

cell intrinsic & cell extrinsic events

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3
Q

The most common extrinsic event that drives cell diversity is _______

A

cell-cell signalling

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4
Q

Types of extracellular signals

A

1) Constitutive signals
2) Mitogens
3) Differentiation signals
4) Apoptotic signals

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5
Q

Constitutive signals do what?

A

maintains the cell

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6
Q

Mitogens do what?

A

tell cells to divide

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7
Q

Differentiation signals do what?

A

tell cell to differentiate

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8
Q

Apoptotic signals do what?

A

tell cells to die

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9
Q

Types of cell-cell communication

A

1) Autocrine
2) Paracrine
3) Juxtracrine
4) Endocrine

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10
Q

Autocrine signaling (def.)

A

cell secrete signaling molecules that act on the cell that secretes

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11
Q

Paracrine signaling (def.)

A

secretion of signaling molecules into extracellular where it acts on the surrounding cells; not contact dependent

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12
Q

Juxtacrine signaling (def.)

A

signaling molecules enter surrounding cells through gap junctions/ membrane nanotubes without secretion into ECM; contact-dependent

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13
Q

Endocrine signaling (def.)

A

signaling molecules are secreted into blood plasma/ECM to act on cells far from the cell that secreted it

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14
Q

Endocrine signaling is only for animals that _____

A

have a vasculature

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15
Q

_____ signaling encourages cells to respond coordinately

A

Autocrine/Paracrine

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16
Q

Most common example of endocrine signaling: ____

A

hormones

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17
Q

Most signaling molecules are _____ and cannot _____ so they ______

A

-hydrophilic
-cross the PM
-interact with cell surface receptors

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18
Q

Signaling molecules that are hydrophobic can ______ and do what? by?

A

-cross the membrane
-cause changes in TF activity
-pairing with intracellular receptor

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19
Q

example of hydrophobic signalling molecule receptor

A

steroid hormone nuclear receptor

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20
Q

Relay proteins do what?

A

pass the message to the next component (protein)

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21
Q

Messenger proteins do what?

A

pass the message to a another part of the cell (ex. cytosol to nucleus)

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22
Q

Adaptor proteins do what?

A

connect one signaling protein to another without a signal

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23
Q

Scaffold proteins are ____

A

a type of adaptor protein that attaches multiple proteins together

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24
Q

Amplifier proteins do what?

A

increase the signal that they receive by producing a lot of intracellular mediators or activating a lot of downstream signaling proteins

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25
Q

Transducer proteins do what?

A

convert the signal into a different form (ex. Phosphorylation signal is used to create cAMP that activates downstream)

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26
Q

Signaling cascade is _____

A

multiple amplification steps

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27
Q

Bifurcation proteins do what?

A

spread the signaling from one pathway to another

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28
Q

Integrator proteins do what?

A

receive signals from two or more signaling pathways and integrate` them

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29
Q

Latent gene regulatory proteins do what?

A

activated at cell surface by activated receptors then move into the nucleus to stimulate transcription

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30
Q

Latent gene regulatory proteins are ____

A

TF that are part of the receptors

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31
Q

Two receptor signals can be integrated if _____

A

-both are needed to activate the same protein
-they activate proteins that interact to propagate downstream signals

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32
Q

general pathway steps

A

1) ligand
2) receptor
3) effector
4) target

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33
Q

NOTCH pathway ligand

A

DELTA

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34
Q

NOTCH pathway receptor

A

NOTCH

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35
Q

NOTCH pathway effector

A

NICD

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36
Q

NOTCH pathway is a ______ signaling pathway

A

paracrine

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37
Q

NOTCH pathway steps

A

1) Delta (attached to adjacent cell) interacts with NOTCH receptor on it EGF-like domains
2) NOTCH receptor (already cleaved at site 1 in the golgi) is cleaved at site 2 and 3 to release NICD tail
3) NICD tail acts as a messenger that goes to nucleus as TF

38
Q

NICD is a part of ______

A

NOTCH receptor that is cleaved when activated by DELTA

39
Q

TGF-B pathway ligand

A

TGF-B

40
Q

TGF-B pathway receptor

A

TGFBR

41
Q

TGF-B pathway effector

A

SMAD

42
Q

TGF-B pathway feedback mechanism

A

target inhibits TGF-B (ligand) & SMAD (effector)(suppress autocrine signaling)

43
Q

TGF-B pathway steps

A

1) TGF-B binds to type II receptor which recruits and phosphorylates type I receptor
2) type I receptor phosphorylate to open smad 2/3 protein
3) smad 2/3 oligomerizes with smad 4
4) smad 2/3 - smad 4 complex migrates to nucleus and activates transcription of target genes

44
Q

WNT pathway ligand

A

WNT

45
Q

WNT pathway receptor

A

Frizzled & LRP (co-receptor)

46
Q

WNT pathway effector

A

B-Catenin

47
Q

WNT pathway transducer

A

GSK3B/Dishevelled

48
Q

WNT pathway scaffold

A

axin

49
Q

WNT pathway (without Wnt signal) steps

A

1) LRP & Frizzled receptor don’t dimerize
2) inactive dishevelled protein
3) active GSK-3B & unstable B- catenin (phosphorylated) held in complex by axin scaffold protein
3) phosphorylated B-catenin is ubiquitylated and degraded by proteasome
4)Wnt responsive genes are off

50
Q

WNT pathway (with Wnt signal) steps

A

1) LRP & Frizzled receptor dimerize
2) activates dishevelled protein
3) active dishevelled protein inactivates GSK-3B & stable B- catenin is unphosphorylated and removed from complex with axin scaffold protein
3) unphosphorylated B-catenin enters nucleus
4)Wnt responsive genes are on

51
Q

Hedgehog pathway ligand

A

hedgehog protein

52
Q

Hedgehog pathway receptor

A

patched

53
Q

Hedgehog pathway transducer

A

smoothened

54
Q

Hedgehog pathway effector

A

GLIA/GLIR (Ci)

55
Q

Hedgehog pathway steps (without HH signal)

A

1) Patched receptor represses smoothened
2) Costal adaptor protein holds Ci/GLI protein + suppressor of Fused + fused protein together
3)Ci protein is ubiquitylated and cleaved by proteasome to form GLIR (repressor)
4)Cleaved Ci + corepressor move to nucleus and repress target genes

56
Q

Hedgehog pathway steps (with HH signal)

A

1) Patched receptor stops repressing smoothened
2) smoothened inhibits proteolysis of GLI and releases Costal adaptor protein + Ci/GLI protein + suppressor of Fused + fused protein complex from microtubule
3)Intact Ci protein (GLIA -activator) + co activator moves into nucleus and activates transcription of target genes

57
Q

Fused and suppressor of fused do what?

A

modify GLI/Ci and lead to proteolytic cleavage

58
Q

GLIA is _____

A

the activator form of GLI/Ci

59
Q

GLIR is ______

A

the repressor form of GLI/Ci

60
Q

_______ (FGF) and ________ (EGF) are part of a protein family of ______

A

-fibroblast growth factor
-epidermal growth factor
-growth factors

61
Q

Growth factor receptors have these extracellular domains which help them to do what?

A
  • cysteine-rich domain and immunoglobulin like domain
    -allows them to bind to growth factors
62
Q

Growth factor receptors have these intracellular domains which help them to do what?

A

-tyrosine kinase domain
-transduce signals into the cell

63
Q

Growth factor (GF) signaling pathway ligand

A

FGF/EGF etc.

64
Q

GF signaling pathway receptor

A

receptor tyrosine kinase (RTK)

65
Q

GF signaling pathway: RTK signals ______

A

AKT & MAPK which signals other TFs

66
Q

GF-RTK signalling pathway steps (MAPK)

A

1) ligand bind leads to clustering of receptors and autophosphorylation of receptor tyrosine kinase domain
2) Grb-2 adaptor protein binds to phos. domain which then binds to Ras-GEF
3) Ras-GEF turns Ras-GDP to Ras-GTP
4) Ras-GTP activates MAP KKK that activates MAP KK –> MAP K with ATP
5) MAP K activates other proteins

67
Q

In GF pathway, RAS proteins acts as ______ to multiple signaling pathways

A

relays and transducers (GTP to phosphorylation)

68
Q

nuclear hormone (steroid hormone) receptor signaling TF is _____

A

the steroid hormone + steroid hormone receptor

69
Q

nuclear hormone receptor signaling: hormone-receptor complex does what in its early primary response?

A

-activates primary response genes in the nucleus

70
Q

nuclear hormone receptor signaling: hormone-receptor complex does what in its delayed secondary response?

A

-primary response protein shuts off primary response genes and turn on secondary response genes to make secondary-response proteins

71
Q

steroid hormones can ______ without ______

A

-cross the PM
-extracellular receptor

72
Q

nuclear receptor superfamily have these domains: _____

A

-transcription-activating domain
-DNA-binding domain
-ligand-binding domain

73
Q

DNA that binds nuclear receptor superfamily has this domain: _____

A

receptor-binding element near the target genes

74
Q

6 types of nuclear receptor superfamily

A

1) cortisol receptor
2) estrogen receptor
3) progesterone receptor
4) vitamin D receptor
5) thyroid hormone receptor
5) retinoic acid receptor

75
Q

Cell diversity in human body needs the production of diverse set of cells when?

A

-during early development and also during adult form for wound healing, hematopoiesis

76
Q

hematopoiesis (def.)

A

blood cell production (all types of blood cell)

77
Q

Neurogenesis (def.)

A

the process by which new neurons are formed in the brain

78
Q

Neurogenesis involves _____ (general)

A

the inactivation of proliferative genes and activation of neurogenic genes

79
Q

proliferative genes do what?

A

encourage the making of more precursor cells

80
Q

TFs involved in neurogenesis

A

-Neurogenin 2
-Bcl6
-Sirt1

81
Q

Neurogenin 2 is what?

A

An activating HLH (helix loop helix) transcription factor that promotes neurogenesis

82
Q

Bcl6 is what?

A

A Zinc-finger transcriptional repressor

83
Q

Sirt1is what?

A

A protein involved in epigenetic repression of
‘active’ chromatin

84
Q

Actions of TFs in Neurogenesis

A

-Sirt1and Bcl6 turn off proliferative genes
-Neurogenin 2 turn on neurogenic genes

85
Q

adipokines (def.)

A

signalling molecules secreted by adipocytes

86
Q

preadipocytes are made from ______

A

mesenchymal stem cells and the absence of Wnt signals

87
Q

adipogenic stimuli does what to preadipocytes?

A

-inhibit pre-adipocyte genes
-inhibit Wnt & B-catenin which normally inhibit further adipocyte differentiation
-activates adipocyte genes

88
Q

how adipocyte genes are activated?

A

-adipogenic stimuli activates C/EBPδ/β which activates C/EBPδ/a & PPARγ which activate adipocyte genes

89
Q

PPARγ is ______ with ______ as activating cofactor. It is highly expressed in _______.

A

-nuclear receptor
-fatty acids
-adipose tissues

90
Q

“Master regulator” of adipogenesis

A

PPARγ

91
Q

C/EBPδ/β is _______

A

-bZip protein

92
Q

Function of C/EBP proteins

A

-integrate proliferation and differentiation genes

CELL 302 (18 decks)

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