Marcu Lecture 8

Marcu Lecture 8 - M arcu Lecture 8 Slide 127 One of the...

Info iconThis preview shows pages 1–3. Sign up to view the full content.

View Full Document Right Arrow Icon
Marcu Lecture 8 Slide 127 - One of the targets of myc/max is kip 1 - Kip1 targets the proteosome to destory p27 - P27 is a class of proteins that negatively regulated the cell cycle o Inhibitor of the kinases that activates cyclins to regulate the cell cycle - Myc/max- without binding DNA can interact with miz1 and prevents it from activating its target genes o Genes are responsible for Inhibitors of cyclin-dependent kinases Slide 131 - Here is miz1 dealing with genes that involved in cell cycle arrest o In p15 and p21 genes - In both cases, mix1 isan essential activator that binds to the promoter of both genes - Absolutely obligatory - When myc is binded to miz1, it is not gonna prevent miz1 from binding to the DNA, but rather, it wont activate transcription - Myc is interfeing with miz1 ability to contact the trasncriptional apparatus - Myc can do this in a complex with max, or without - You don’t really need max for this, it is only needed if myc wants to bind DNA Slide 129, 130 - Carboxytermina of myc is the DNA binding domain through helix-turn-helix motif - Max and miz1 both interact with CTD of myc, but the amino acid interactions are different for each o Max interacts by helix-loop helix- o Miz1 interacts with the few amino acids very close to the basic region that contact DNA - In its activation domain, it can also interat with sp1 whih is a zinc-finger protein - Has a couple of distinct activation domains and 1 DNA binding domain o MBI and MBII - This allows it to bind multiple co-activators: p400, TRRAP, SKP2, ptefb - Also interacts with a mediator - Depending on what the gene needs will determine which co-activators bind Slide 133 - Not responsible for this slide - Intricacies of myc control and regulation of many other genes by miRNAs
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full Document Right Arrow Icon
- You don’t want a lot of myc transcription because you start to induce cell death Slide 136 - What activates of myc - Levels of myc in the cell are usually low, half lifes are short - Much of the regulation of myc is determine by turnoever tof the protein and turnover of the messenger protein o Most based on post-trasncriptional control o But also in trasncriptional control as well - Deregulated levels of transcription usually leads to cancer cells which usually signals for p53 Slide 134 - Signal transduction pathway of beta catenin that controls myc - Tcf Lef are transcriptional activators that bind to the myc promoter - However, they don’t work unles they have their co-activator protein which is beta- catenin - Betat cantenin is a small protein held in check in the cytoplasm by a protein complex that uses a proteosome to keep levels low
Background image of page 2
Image of page 3
This is the end of the preview. Sign up to access the rest of the document.

{[ snackBarMessage ]}

Page1 / 6

Marcu Lecture 8 - M arcu Lecture 8 Slide 127 One of the...

This preview shows document pages 1 - 3. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online