Nicknamed the guardian of the genome, this tumor suppressor protein is a DNA binding protein that regulates transcription. Its domains are cell cycle regulation and DNA repair. Mutations of the p53 gene are found in 50% of all cancers. After DNA damage occurs, ATM (ataxia telangiectasia mutated) activates p53, which activates p21, GADD45, and, if necessary, BAX. P21 is a cyclin dependent kinase inhibitor, and it does G1 arrest, stopping the cell in G1 phase from proceeding to S phase. GADD45 repairs DNA damage. BAX signals apoptosis. MDM2, an ubiquitin ligase, stops p53 by ubiquinating it and so sending it to the proteasome. ARF/p14 inactivates MDM2. USP7, an ubiquitin specific protease, takes off the ubiquitin on p53. Radiation, a common treatment of cancer, won’t work on cancers including a mutation of p53. Epstein-Barr virus releases EBNA-1, which inactivates USP7. HPV uses E6 to ubiquinate p53 and E7 to take the place of E2F, which contain info for transcription enzymes, under the retinablastoma.
Tonight I'm going to write down every thought I have while writing this study essay
- Why do I have to write this?
- Recessive? Getting cancer is recessive? Can I make an argument that people with mostly dominant features will not get cancer as much?
- No, that’s a stupid idea. Mutations….like zombies??
- YES!!!! One paragraph in 30 minutes? NAILED IT
- Wait, can I cure cancer?
- Oh my gosh……I caused my dad’s cancer. I’m going to die now.
- I hate this
- What’s my thesis again??….OH YEAH!!!! **click click click**
- FINISH IT!!!! FOR SPARTA!!!!!!!!!!!!!!
- Why am I listening to the Harry Potter and Alice in Wonderland score???
- Conclusion…..how to do a conclusion……
- AH YEAH!!!! UNDER 3 HOURS!!!!!!!
- I hate everything that is cancer
p53 supporting tumor growth? gasp
“Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells”
Serine is an essential amino acid that can be converted to glycine, while simultaneously replenishing me-THF. It seems that tumors require p53 to maintain proliferation in the absence of serine… therefore p53-/- tumors are actually more sensitive to serum starvation than p53+/+.
I will re-read this paper after I review my metabolic pathways notes.. ughhh