Seminario 22 Salida del ciclo celular y muerte celular - Federico Waisberg

Hello, my name is Federico Weisberg. Okay, let's look at the first of the topics I'm assigned, which is exit from the cell cycle and cell death. As a review of the cell cycle, we had seen in the course that the G1S entry was caused by the accumulation of cyclin D. When we had an accumulation of cyclin D, cyclin-

dependent kinase 46 could act and this could trigger retinoblastoma hyperphosphorylation. When retinoblastoma was hyperphosphorylated, the transcription of elements that are necessary in the phase stage such as cyclin E was allowed. With the cell cycle started there are typical responses to AD damage. These are recognized by mediator proteins such as ATM, ATR, Check2 and Check 1, which can respond

to double-strand damage, nucleotide damage, nucleotide mismatch alterations and trigger some possible response to try to repair the damage. One is repair, the other is the rapid inhibition of cyclin-dependent kinases, for example, by activating phosphates. And the third is by increasing the half-life of P53. P53 is the guardian of the genome and tends to

degrade rapidly. If some of these proteins that are related to damage are phosphorylated or detect damaged DNA, P53 will become phosphorylated and act as a transcription factor for multiple targets. One of the main ones is from Puma and Noxa, which, as we will see today, participate in the intrinsic pathway of apoptosis. It

will also generate the transcription of P21 which, by interacting with cyclin-dependent kinase , especially 2, will arrest the cell cycle. It will also condition the epigenetic modification to generate the phenotype of sensibility, which we will see today, and even trigger some proteins such as MGMT, the polymerase layer, which will favor some repair pathways.