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Applied Biochemistry > Cell Signaling Pathways Growth Factors > Flashcards

Cell Signaling Pathways Growth Factors Flashcards

1
Q

what are growth factors?

A

substances capable of inducing cell growth, proliferation, healing, and/or differentiation

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2
Q

what are the major types of growth factors? (2)

A

proteins and steroids

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3
Q

signaling of growth factors involves

A

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

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4
Q

what are the major families of growth factor receptors? (3)

A

tyrosine kinase activity
seine/threonine kinase activity
G protein coupled receptor

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5
Q

nerve growth factor (NGF) signaling pathway

A

Binding interaction between NGF and the TrkA receptor facilitates receptor dimerization and tyrosine residue phosphorylation of the cytoplasmic tail by adjacent Trk receptors. Trk receptor phosphorylation sites operate as Shc adaptor protein docking sites, which undergo phosphorylation by the TrkA receptor. The Trk receptor complex recruits a second adaptor protein called growth factor-receptor bound protein-2 (Grb2) along with a docking protein called Grb2-associated Binder-1 (GAB1) (not shown). Subsequently, phosphatidylinositol-3 kinase (PI3K) is activated, resulting in Akt kinase activation.

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6
Q

TrkA

A

tropomyosin receptor kinase A

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7
Q

TrkA is a high affinity receptor involved in

A

neuronal differentiation and preventing cell death

survival genes

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8
Q

p75

A

neurotrophin receptor

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9
Q

p75 is raining expressed in early

A

neuronal development

promote apoptosis

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10
Q

EGF signaling pathway

A

Signaling pathways and inhibitors of EGFR. Activation of EGFR leads to homodimerization/heterodimerization, phosphorylation of specific tyrosine residues, and recruitment of several proteins at the intracellular portion of the receptors. Phospholipase Cγ (pink) and STAT transcription factors (blue) bind directly to the receptor, whereas Ras/Raf/MAPK pathway (orange) and PI3K pathway (green) need several specific adaptor molecules (yellow). PI3K can also bind directly any of the erbB partners of EGFR heterodimers. Concomitantly, the activated receptors undergo endocytosis and follow two possible routes: lysosomal degradation or importin-mediated nuclear translocation. Once in the nucleus, EGFR can either behave as a proper transcription factor (for cyclin D1 up-regulation) or as coregulator of other gene transactivators. Both pathways result in nuclear activation of genes related with cell proliferation, survival, invasion, and metastasis. Two main strategies are available for EGFR kinase inhibition: mAb and small-molecule TKIs. mAbs act extracellularly, avoiding EGFR ligands binding, whereas TKIs compete with the ATP binding to the kinase domain of the receptor. DAG, 1,2-diacylglycerol; IP3, inositol 1,3,5-triphosphate; PLCγ, phospholipase Cγ; Erk-1, extracellular signal-regulated kinase-1; Erk-2, extracellular signal-regulated kinase-2; FAK, focal adhesion kinase; PKC, protein kinase C.

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11
Q

TGFb subfamilies (4)

A

TGFb subfamily
decapentaplegic (Dpp, Drosophila) related subfamily including BMPs and growth differentiation factors
action and inhibit subfamily fourth subfamily of diverse members

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12
Q

BMPs

A

bone morphogenetic proteins

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13
Q

action and inhibin subfamily regulate

A

sex organ development

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14
Q

genes for many growth factors or their receptors are

A

proto-oncogenes

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15
Q

not all proto-oncogenes encode growth factors. many encode

A

transcription factors

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16
Q

how are the majority of growth factors translated?

A

as a pro-form and then undergo proteolytic processing steps by members of the pro protein convertase family of enzymes

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17
Q

how many members are there of the pro protein convertase family?

A

9

furin is the best studied

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18
Q

dr. forsake has studied — for many years

A

SKI-1 (important for processing with SREBP)

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19
Q

furin

A

cleaves a number of pro proteins

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20
Q

Turin is involved in (4)

A

neuronal innervation
control of juxtacrine versus paracrine signaling
cartilage breakdown
tumor metastasis

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21
Q

steps of synthesis of TGFb (7)

A

TGFb precursor
dimerization and cleavage
small latent complex
large latent complex moves from the cytosol to the ecm
stored associated with eco through binding of the RGD motif to alpha integrins
proteases cleave
TGFb is released

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22
Q

TGFb ligands are active as

A

homo or heterodimers

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23
Q

homo/heterodimer

A

two polypeptide chains linked by a single disulfide bond

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24
Q

ligand binds to a type 2 receptor, which will

A

recruit a type 1 receptor subunit

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25
Q

type 2 receptor is a

A

serine/threonine kinase

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26
Q

binding of the ligand results in the

A

phosphorylation of the recruited type 1 receptor

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27
Q

in the canonical or classical pathway, the type 1 receptor then phosphorylates a receptor regulated

A

SMAD protein

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28
Q

how many type 1 receptors and type 2 receptors are there in mammals?

A

1: 7
2: 5

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29
Q

the canonical or classical pathway serves to initiate a

A

SMAD dependent intracellular signaling cascade that activates or inhibits gene transcription

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30
Q

myostatin

A

inhibitor of muscle growth

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31
Q

growth factors and cytokines affecting various steps in wound healing include (6)

A 
fibroblast migration/replication
keratinocyte replication
angiogenesis 
collagen synthesis 
collagense secretion
monocyte chemotaxis
32
Q

why do dogs lick their wounds?

A

their saliva is rich in TGFb which starts the wound healing process

33
Q

wound healing

A

complex process in which skin or other tissue repairs itself after injury

34
Q

the classic model of wound healing can be divided into four sequential overlapping phases:

A

hemostasis
inflammatory phase
proliferative phase
remodeling phase

35
Q

hemostasis

A

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

36
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

37
Q

proliferative phase

A

angiogenesis, collagen deposition, granulation tissue ormation, epithelialization, and wound contraction

38
Q

remodeling phase

A

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

39
Q

examples of disease states which can interfere with wound healing progression (4)

A

diabetes
venous or arterial disease
old age
infection

40
Q

diabetic ulcers

A

diabetic wounds do not heal quickly, sometimes don’t even realize they have a wound

41
Q

hemostasis involves

A

platelets

42
Q

inflammatory phase involves (3)

A

monocytes
neutrophils
macrophages

43
Q

proliferative phase involves (3)

A

fibroblasts
endothelial cells
keratinocytes

44
Q

remodeling involves

A

fibroblasts

45
Q

BMP segnalino involves

A

SMADs

46
Q

SMADs result in

A

regulation of gene expression

47
Q

how is growth factor expression restricted? (2)

A

temporarlly and spatially

48
Q

how was it shown that growth factor expression is temporally and spatially separated in craniofacial growth and development?

A

transgenic mice expressed the lac z gene which is regulated by a BMP4 receptor. wherever BMP4 is lac z is expressed, which stains embryos with a blue dye, which shows BMP4 expression in different regions (expressed at different times and spaces in development)

49
Q

fracture healing involves

A

spatial and temporal restricted expression of multiple BMPs

50
Q

growth factors often work in combination to achieve

A

complex structures of growth and differentiation

51
Q

salivary gland branching morphogenesis involves multiple

A

growth factors expressed spatially and temporally

52
Q

do all growth factors stimulate growth?

A

no

53
Q

TNF

A

tumor necrosis factor

54
Q

TNF mediates

A 
death pathways 
(intracellular signaling events lead to change in gene expression and cell death via apoptosis
55
Q

what types of therapeutic options can be placed in the periodontal defect? (4)

A

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

56
Q

why are these substances used to treat periodontal defects?

A

they’re packed with growth factors to stimulate growth

57
Q

why are these substances used to treat periodontal defects?

A

they’re packed with growth factors to stimulate growth

58
Q

BMP2 mutation

A

brachydactyly type A2, mutation in 3’-regulatory element suggestive of a long range regulator of transcription

59
Q

BMP4 mutations (2)

A

microphthalmia, eye, brain, and digit developmental abnormalities
orofacial cleft, microform cleft lip and cleft palate

60
Q

BMP15 mutation

A

ovarian dysgenesis 2, hypergonadotropic ovarian failure

61
Q

BMPR, type 2 mutation

A

pulmonary hypertension

62
Q

Loeys-Dietz syndrome

A

caused by a mutation in the TGF-β receptor-1 and TGF-βreceptor-2. Autosomal dominant mutation causing widely spaced eyes, cleft palate or bifid uvula, and aortic aneurysms

63
Q

Camurati-Engelmann disease

A

autosomal dominant mutation in TGF-b1 causing progressive diaphyseal dysplasia (hyperostosis and sclerosis of diaphyses of long bones)

64
Q

Colorectal cancer hereditary nonpolyposis

A

mutations in TGF-β receptor-2

65
Q

Arrhythmogenic right ventricular dysplasia 1

A

mutation in TGF-β3

66
Q

PDGF-beta- dermatofibrosarcoma protuberans

A

Due to genetic rearrangement, PDGF-beta is produced without its normal regulation giving rise to tumor formation

67
Q

IGF1Rl

A

mutation in IGF-receptor which causes resistance to IGF-1. Leads to intrauterine growth retardation and short stature

68
Q

NGF

A

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

69
Q

inflammatory bowel disease

A

chronic relapsing intestinal inflammation

70
Q

two kinds of inflammatory bowel disease

A

chrons disease

ulcerative colitis

71
Q

chrons and ulcerative colitis are both classified as

A

autoimmune diseases

72
Q

what plays a key role in chronic inflammation?

A

TNFa

73
Q

inflammatory bowel disease treatment

A

monoclonal antibodies, infliximab and adalimumab, which are directed against TNFa and prevent its binding to its receptor

74
Q

rheumatoid arthritis

A

chronic inflammation

75
Q

chronic inflammation can be treated with

A

an antibody against TNFa or other type of inhibitor

76
Q

etanercept (Enbrel)

A

recombinant fusion protein between the TNFa receptor and the constant region of the IgG1 antibody, which binds TNFa and prevents its cellular action

Applied Biochemistry (52 decks)

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