ENVB 437 Lecture Notes - Lecture 15: Class Action, Brain Tumor, Supercomputer
4 Jun 2018
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Eukaryotic cells and viruses – lecture 15 (February 28th, 2018)
Slide 82 – Cell cycle check point G1/S
- The normal course of events is that if any reason the cell is stressed, we induce the activation of p53 so the
phosphorylated tetramers form and they act as transcription factors to indiuce other genes
o P21
▪ When complexes to an activated CKD – it blocks its activity
• Normally it would phosphorylate Rb and in its phosphorylated form it doesn’t form
the association with E2F
• Involved in nucleotide synthesis DNA synthesis etc and you go from G1 to S and you
cant stop
▪ The idea is to repair DNA and then replicate
- When E6 and 7 are expressed ast high levels:
o E6 inactivates p53 so you cant induce genes such as p21
o E7 can bind rb and that alters the conformation and destroys the association
find more resources at oneclass.com
find more resources at oneclass.com
Slide 83 – oncogenesis associated with human viruses
- Epstein-Barr associated with LMP-1 for example
o (see image for others)
- HBV can get integrated…
o Or it can go an indirect route similar to HCV
▪ Leads to chronic inflammation or various protein
• Tumour formation
• Inhibition of apoptosis
Slide 84
- Acute reaction and normally those are
cleared from the system
- If it persistes, that can result in a chronic
inflammation
o You also have other disruptions in
metabolism that can result in
DNA damage → free radicals
▪ Can result in the
promotion of cells from a
precancerous to a
cancerous state over time
▪ Looking for additional
damage to fully transform
a cell
find more resources at oneclass.com
find more resources at oneclass.com
Slide 85 – SV-40 Virus genome
- 40th monkey virus discovered
- about 5 kb ds circular DNA
o Small genome simian virus
▪ Has overlapping reading frames and it reads in two
directions as indicated by the aarrouws going in
different directions
o Codes for 6 genes
o Papovavirus
o oncogenic DNA virus in primate cells
o model system for mammalian DNA replication
- Large T antigen is an “early” gene (DNA helicase)
o Helicase is unwinding the DNA for replication normally
Slide 86 – Large T antigen
- Problems arise when helicase activity also has binding sites to both retinoblastoma and p53
- You are inhibiting those tumour suppressor genes and this can cause the cell to replicate when it has DNA
damage etc
- It also promotes the transcription of various genes as well as various growth facots
- Normally doesn’t cause a problem in humans
o It was a contaminant of early polio
vaccines
o People who were mandatorily vaccines
against polio also were getting SP40
▪ SP40 is also a co-carcinogen
with asbestos
• Which a lot of people
were using in houses
- Increases cell division/decreases
- apoptosis therefore cell accumulates
- additional mutations – tumour
- Also increases transcription of growth promoting genes e.g. IGF1, telomerase
- Interactions with asbestos fibers and SV40 have been reported i.e. co-carcinogens
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Eukaryotic cells and viruses lecture 15 (february 28th, 2018) Slide 82 cell cycle check point g1/s. Involved in nucleotide synthesis dna synthesis etc and you go from g1 to s and you cant stop: the idea is to repair dna and then replicate. When e6 and 7 are expressed ast high levels: e6 inactivates p53 so you cant induce genes such as p21, e7 can bind rb and that alters the conformation and destroys the association. Slide 83 oncogenesis associated with human viruses. Epstein-barr associated with lmp-1 for example (see image for others) Hbv can get integrated : or it can go an indirect route similar to hcv, leads to chronic inflammation or various protein, tumour formation. Acute reaction and normally those are cleared from the system. If it persistes, that can result in a chronic inflammation: you also have other disruptions in metabolism that can result in.
