lecture 5

lecture 5 - Lecture #5 Tuesday 4/15/08 -1- Announcements: -...

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Lecture #5 – Tuesday 4/15/08 - 1 - Announcements: - Webct . A folder named “Reading Material Not Required” has been added. It contains 2 articles now, with more to be added each week. This is required reading that may or may not be tested on. It’s interesting stuff, so take some time to read it. Last lecture: Growth factor (GF) signaling, angiogenesis and its signaling. This lecture: Signal transduction pathways and tumor suppressor genes/growth factor signaling and how it influences tumor formation. Signaling – Usually think of an external ligand binding a receptor on the plasma membrane, effecting cytoplasmic signal pathways, effecting nuclear changes (transcription factors), etc. - There are genes involved in malignancy that represent each step. Nucleus out: Transcription Factors (TF) – There aren’t many involved in malignancy/tumor formation directly, indirectly is another story (increase tyrosine kinase activation in a mutant receptor, etc). Transcription factors that act as oncogenes: - AP-1 factors: a TF is a protein that binds an enhancer element in DNA, increasing transcription of genes downstream of its target genes. o Factor consists of 2 families of proteins that heterodimerize with one another and then ultimately bind to DNA: c-fos and c-jun (c for cellular) - c-Fos and c-Jun were popular genes to study in the mid-late 80s because of a single observation that classified them in a class called Immediate Early Genes. o These were genes that were turned on within seconds when quiescent (non-growing) cells were stimulated with growth factors. o Why important? How were they studied? - System: immortalized 3T3 cell line. - Removed all serum from media and just had tissue culture media (no GF’s or barely enough to keep cells alive). Could induce a state of quiescence the cells are not senescent, they just stop growing. What gets turned on when a cell like these see a GF? - Add serum back and look at genes within minutes of stimulation. - Found a set of genes called the master control genes . At top of pyramid that turned everything else on - c-fos and c-jun came up early, therefore people argued that these were master control genes. o Master control genes = Immediate Early genes. c-Fos: Turns on within seconds after adding GF’s. - Was isolated from v-fos (specifically an Avian virus that causes bone tumors in birds, potent TF that influences bone development) - If it’s an immediate early gene, when knocked out (KO) in mice: o Expect to see: mouse might pass fertilization stage and maybe 4-8 cell stage of zygotic division but then die.
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Lecture #5 – Tuesday 4/15/08 - 2 - o Actually saw: Mice were fine, but had no teeth. - From this, researchers argued that it’s not enough just to look at the time frame of gene activation, need to also look at their target genes of the TF’s, how important are those genes for the overall biology of the cell, how important they are for driving malignancy, but they are not central or clear cut. How did c-fos and c-jun get turned on?
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This note was uploaded on 07/21/2008 for the course BIMM 134 taught by Professor Johnson during the Spring '08 term at UCSD.

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lecture 5 - Lecture #5 Tuesday 4/15/08 -1- Announcements: -...

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