growth factors Flashcards
what do growth factors stimulate and how does it work
. cellular growth
. proliferation
. regeneration
. cellular differentiation
they bind to target cells by specific receptors on cell membrane
growth factors examples
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 does growth factor allow cell to grow
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.
what do embryonic pluripotent stem cells
differentiates into endo, ecto, mesoderm + unlimeted self renewal capacity
***but eithical issues so scientists use induced pluripotent stem cells.
what are iPSCs
manipulated somatic cells (undifferentiated) but are able to differentiate
with growth factors they turn into progenitor cells (organ/tissue development)
What Organoids used for
. 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
parts of a 3D bioprinting sytstem and what it does
. controller
. dispensing module
. closed acrylic chamber wth temp controller + humidifier
to imitate target tissue/organs
in tumour suppressor genes if mutated, is it recessive or dominant mutation.
Under what conditions
recewssive allele
As long as cell contains 1 normal alelle, tumour suppression continues
Mutations in individuals with heterozygous tumour suppressor gene
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.
What is retinoblastoma and what can it do
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)
What are the 2 forms of Rb
Dephosphorolated= inhibits replication and forbids mitosis
Phosphorylated= When permission given, it tuns into Phosopho-Rb and liberated cell replcation and aloows mitosis
What is E2F
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 is the activation chain for DNA rplication
- 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.
Why the mutant recessive Rb may behave as dominant?
Loss of heterozygosity
P53 is a tumour suppressor gene like Rb.
What happens if a person only inherits 1 functional copy
Li Frsaumeni syndrome
You are predisposed to ccancer