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Biochem Quiz #2 (part 1/2 for exam #2) > 9/20/21 Cell Signaling Pathways: Growth Factors > Flashcards

9/20/21 Cell Signaling Pathways: Growth Factors Flashcards

1
Q

What are growth factors?

A
  • Substances capable of inducing cell growth, proliferation, healing and/or differentiation
  • major types are proteins and steroids
  • critical roles: embryonic development and repair processes of human tissues and organs.
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2
Q

Growth factor signaling involves what?

A

Signaling involves binding to a cell membrane receptor and then activation of various intracellular signaling pathways

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3
Q

what are the major families of growth factor receptors

A

with tyrosine kinase activity, serine/threonine kinase activity, and G-protein coupled receptors.

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4
Q

what are the 2 main nerve growth factor receptors?

A
  1. TrkA

2. p75 NTR

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5
Q

TrKA receptor role and goal

A
  • facilitates receptor dimerization and tyrosine residue phosphorylation of cytoplasmic tail
  • goal: activation of genes promoting survival
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6
Q

p75 NTR role and goal

A
  • initiates NFkB and JNK

goal: activation of gene promoting survival and apoptosis

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7
Q

Epidermal Growth Factor Signaling

A

Activation of EGFR leads to homo/heterodimerization, phosphorylation of specific tyrosine residues, and recruitment of several proteins at the intracellular portion of the receptors.

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8
Q

TGF-β Superfamily and its 4 major subfamiles

A

One of the largest groups of cell regulatory proteins

  1. TGF-beta subfamily
  2. Decapentaplegic (Dpp) and growth differentiation factors
  3. Activin and inhibin subfamily (they regulate sex organ development)
  4. diverse members
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9
Q

what type of gene is for many growth factors or their receptors?

A

proto-oncogenes

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10
Q

do all proto-oncogenes encode transcription factors?

A

no, but many do

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11
Q

majority of growth factors are translated into what?

A

a pro-form and then undergo proteolytic processing steps of the proprotein convertase family of enzymes.

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12
Q

There are 9 members of the proprotein convertase family, which one is studied best?

A

furin

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13
Q

furin cleaves a number of proproteins. what are the 4 different ways?

A
  1. neuronal innervation
  2. control of juxtacrine vs. paracrine signaling
  3. cartilage breakdown
  4. tumor metastasis
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14
Q

neuronal innervation

A

furin cleavage of pro-B-NGF results to neuronal innervation & survival

NO furin cleavage->apoptosis

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15
Q

control of juxtacrine vs. paracrine signaling

A

furin cleavage of Eda-1 undergoes paracrine signaling to reach target cell

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16
Q

cartilage breakdown

A

furin cleavage-> active ADAMTS-4-> degradation of cartilage protein ->rheumatoid arthritis

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17
Q

tumor metastasis

A

furin cleavage of pro-MT1-MMP-> tumor metastasis

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18
Q

TGF-β synthesis (intracellular)

A
  1. TGF-β precursor
  2. Dimerization & cleavage
  3. Small Latent Complex
  4. Large Latent Complex
  5. Secretion
  6. Stored assoicated with extracellular matrix thru RGD motif binding to αv integrins
  7. Active TGF-β is released
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19
Q

how are TGF-β ligands active?

A

as homo- or heterodimers, two polypeptide chains linked by a single disulfide bond.

(They initially bind to a specific type II receptor subunit, which recruits a type I receptor subunit. )

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20
Q

Type II receptor of TGF-β

A
  • serine/threonine kinase.

- binding of ligand results in the phosphorylation of the recruited type I receptor.

21
Q

how does type I receptor of TGF-β act in canonical or classical pathway?

A

phosphorylates a receptor regulated SMAD protein.

22
Q

canonical or classical pathway

A

to initiate a SMAD-dependent intracellular signaling cascade that activates or inhibits gene transcription

23
Q

think SMAD as

A

TGF-β

24
Q

what is a member of the TGF-β Superfamil?

A

Myostatin (GDF8)

25
Q

wound healing

A

Complex process in which skin or other tissue repairs itself after injury.

26
Q

what are the 4 sequential phases of wound healing?

A
  1. homeostasis
  2. inflammatory phase
  3. proliferative phase
  4. remodeling phase
27
Q

hemostasis

A

within minutes post-injury, platelets aggregate at the injury site to form a fibrin clot which acts to control bleeding.

28
Q

Inflammatory phase

A

bacteria and debris are phagocytosed and removed from the wound site. Factors are released that cause migration and division of cells involved in the proliferative phase.

29
Q

Proliferative phase

A

angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction.

30
Q

Remodeling phase

A

collagen is remodeled and realigned along tension force lines and cells no longer needed are removed by apoptosis.

31
Q

what disease states can interfere with wound healing progression?

A

diabetes, venous or arterial disease, old age, infection

32
Q

diabetic ulcer

A
  • can occur in mouth and feet
  • diabetics can have difficulty with wound healing
  • some may not notice the ulcer
33
Q

Canonical BMP signaling

A

SMADs—intracellular proteins that transduce extracellular signals from transforming growth factor beta and BMP ligands to the nucleus where they activate downstream gene transcription.

34
Q

During craniofacial growth/ development, how does growth factor expression act?

A

it is temporally and spatially restricted

- different BMP expressions

35
Q

how do growth factors work to achieve complex structures of growth and differentiation?

A

work in combination

36
Q

signaling in tooth development steps?

A

initiation->morphogenesis-> differentiation & mineralization-> root formation & eruption

37
Q

Salivary gland branching morphogenesis involves what?

A

multiple growth factors expressed spatially and temporally

38
Q

what growth factor does NOT stimulate growth?

A

Tumor necrosis factor (TNF) mediates death pathways

39
Q

Treatment of Periodontal Defects

A

Therapeutic options:

bone grafts, enamel matrix derivative (EMD), platelet-derived growth factor (PDGF) or platelet-rich plasma (PRP),

40
Q

genetic diseases are due to what MAIN growth factor mutations?

A

BMPs and TGF-β

41
Q

genetic diseases are due to what OTHER growth factor mutations?

A

PDGF-beta
IGF1RI
NGF

42
Q

PDGF-beta mutation

A

dermatofibrosarcoma protuberans.

giving rise to tumor formation.

43
Q

IGF1Rl mutation

A

causes resistance to IGF-1. Leads to intrauterine growth retardation and short stature

44
Q

NGF mutation

A

hereditary sensory and autonomic neuropathy. Mutation causing loss of deep pain and temperature perception

45
Q

Inflammatory Bowel Disease and its treatment

A

chronic relapsing intestinal inflammation, growth factor-related disease

treatment: monoclonal antibodies, infliximab and adalimumab, which are directed against TNF-alpha and prevent its binding to its receptor.

46
Q

what two kinds of diseases are associated with inflammatory bowel disease and are classified as autoimmune disease?

A

Crohn disease and ulcerative

47
Q

what plays a key role in chronic inflammation?

A

TNF-alpha

48
Q

Rheumatoid arthritis and its treatment

A

also involves chronic inflammation, growth factor related disease

treatment: an antibody against TNF-α or other type of inhibitor (ig. Etanercept)

49
Q

Etanercept (Enbrel)

A

under Rheumatoid arthritis treatment ;
a recombinant fusion protein between the TNF-α receptor and the constant region of the IgG1 antibody; which binds TNF-α and prevents its cellular action.

Biochem Quiz #2 (part 1/2 for exam #2) (4 decks)

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