Talk:2016 Group Project 1: Difference between revisions
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Just trying to simplify and understand the process some of my notes !(z3417363) | ==Notes== | ||
Just trying to simplify and understand the process and these are some of my notes !(z3417363) | |||
The inactive Wnt Pathway In a normal cell: | The inactive Wnt Pathway In a normal cell: |
Revision as of 20:44, 12 September 2016
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Signalling: 1 Wnt | 2 Notch | 3 FGF Receptor | 4 Hedgehog | 5 T-box | 6 TGF-Beta | |||
Here are some starting places for the topic. Can be patterning, differentiation, etc. as long as a developmental signal process/pathway. |
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To all group members:
- More info on pathway focusing on fetus development, and which pathway it is majorly part of - focus research on those body parts
- Make your section presentable
- At least one picture per section
Notes
Just trying to simplify and understand the process and these are some of my notes !(z3417363)
The inactive Wnt Pathway In a normal cell:
In most normal cells the Wnt pathway is inactive. In the cytosol , the destruction complex is formed from the proteins beta catenin, GSK3 beta, Axin,APC, Ck1-alpha. The ubiquitin ligase beta TRCP is able to bind to beta catenin and transfer short ubiquitin peptides to beta-catenin. In other words the beta-catenin is phosphorolated and this beta catenin can then bound and be by a complex of protease (proteasome) . Thus a low level of cellular beta catenin is achieved. Therefore no beta catenin reaches the nucleus and the transcription factor of the TCF LEF family along with other proteins (groucho) binds to DNA and inhibits gene expression. So essentially when WnT is inactive, beta canenin is destroyed and does not reach nucleus and transcription is inhibited.
The Active Wnt Pathway in a normal cell.
Extracellular(outside cell) Wnt binds with the membrane receptor frizzled (FZD). The wnt pathway is activated and activates the cytosolic protein "dishevelled"(DSH) which induces dissociation of the protein destruction complex. Because the protein complex is destroyed beta- catenin is no longer modified by unbiquitin peptides/phosporolated and is not destroyed. Since the supply of beta catenin continues the level of beta catenin rises, first in the cytosol and later in the nucleus. Once the beta catenin reaches the nuclue it binds to the TCF LEF transcription factor which changes them from a transcriptional repressor into an activator. TCF itself activates an RNA polymerase which induces gene transcription. So essentially WnT starts gene transcription by allowing beta catenin to reach the nucleus.
This is actually very similar to a tumour cell where the mutation of the protein complex also inhibits the destruction of beta catenin and allows it to grow in quantity and reach the nucleus and start gene expression. However this is not uncontrolled and can be compared to a car travelling with no brakes. Ultimately this abnormal proliferation leads to malignant adenocarcinoma (cancer).