growth factors Flashcards

1
Q

what do growth factors stimulate and how does it work

A

. cellular growth
. proliferation
. regeneration
. cellular differentiation

they bind to target cells by specific receptors on cell membrane

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

growth factors examples

A

KGF - Growth + new keratinocyte gen

PDGF - growth, new gen, repairs blood vessels, collagen prod (platelet derived)

VEGF - promotion of angiogenesis + wound healing ( vascular endothelial)

EGF - promotion of epithelial cell growth, angiogenesis + wound healing (epidermal)

FGF - present in epithelialization phase of wound healing. keratinocytes cover wound making epithelium. (fibroblasts)

IGF - cell growth regulation (insulin)

TGF-B - growth + neogenesis of epithelial cells + vascular endothelial cells. prom wound healing (transforming beta)

CTGF - promotes angiogenesis, cartilage regen + platelet adhesion (connective tissue)

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

how does growth factor allow cell to grow

A

contact btw GF + receptor stimulates enzyme activity of cytoplasmic domain of receptor.
signal gets to nucleus, genes then resposible to start replication + prep for mitosis
proteins for g1-s transition made.

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

what do embryonic pluripotent stem cells

A

differentiates into endo, ecto, mesoderm + unlimeted self renewal capacity
***but eithical issues so scientists use induced pluripotent stem cells.

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

what are iPSCs

A

manipulated somatic cells (undifferentiated) but are able to differentiate
with growth factors they turn into progenitor cells (organ/tissue development)

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

What Organoids used for

A

. normal organ development
. pathology in organ development
. drug effects

they can self organize therefore mimic general tissue structure + development found in IN VIVO. also in them, diff cells can help eachother to differentiate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

parts of a 3D bioprinting sytstem and what it does

A

. controller
. dispensing module
. closed acrylic chamber wth temp controller + humidifier

to imitate target tissue/organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

in tumour suppressor genes if mutated, is it recessive or dominant mutation.
Under what conditions

A

recewssive allele

As long as cell contains 1 normal alelle, tumour suppression continues

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

Mutations in individuals with heterozygous tumour suppressor gene

A

Mutation causes the normal copy of the gene to become mutated = LOSS OF HETEROZYGOSITY

so cell turns into cancer cell

That is why, at the cell level mutations
in tumor suppressors are recessive,
but for the whole organism they are
dominant.

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

What is retinoblastoma and what can it do

A

Retinoblastoma Rb is a tumour suppressor gene

It can: inhibit cell division without permission, inhibit cell division even when permission for mitosis is given ( cell doesnt complete requirements for mitossi eg damaged DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 forms of Rb

A

Dephosphorolated= inhibits replication and forbids mitosis

Phosphorylated= When permission given, it tuns into Phosopho-Rb and liberated cell replcation and aloows mitosis

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

What is E2F

A

Transciptional factor that triggers expression of set of genes to start DNA replication

If there is no signal to start
mitosis, Rb blocks E2F.
Phospho

-Rb liberates E2F.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is the activation chain for DNA rplication

A
  • growth factor binds onto receptor of cell
  • Receptor activated in cytoplasmic region
  • Causes activation of protein kinases in cytoplasm
  • One of the activated kinases enters the nucleus and adds
    phospho groups to Rb.
  • Phospho-Rb liberates E2F.
  • Replication is triggered.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why the mutant recessive Rb may behave as dominant?

A

Loss of heterozygosity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

P53 is a tumour suppressor gene like Rb.
What happens if a person only inherits 1 functional copy

A

Li Frsaumeni syndrome
You are predisposed to ccancer

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

If P53 is activated, what can it do

A
  • Cell cycle arrest for DNA repair
  • Apoptosis to discard damaged cells
17
Q

Protooncogenes vs oncogenes

A

Proto oncogenes code for proteins that positivily stimulate cell cycle

They can become oncogenes due to mutations or overexpression=cause tumour

18
Q

How can a proto oncogene lose its function

A
  • Change in protein structure causing increase in protein activity
  • gene duplication/amplification
  • loss of regualtion
19
Q

Do oncogene behave as dom or rec
Are they only due to mutations/overexpression of protooncogenes

A

Behave as dominant= 1 mutant allele predisposes to tumour form

Oncogenes can be introduced into cells by onconogenic viruses