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Team:BrownTwo/Limiter/utility
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<p>Much as excessive signal levels can destroy a radio transmitter, excessive genetic expression can cause damage in living systems. While cells are usually well-equipped to modulate their own transcriptional behavior, an investigation into pathological gene expression indicates that many situations arise wherein the expected regulatory response fails. Our device is designed to augment endogenous gene regulatory pathways.</p> | <p>Much as excessive signal levels can destroy a radio transmitter, excessive genetic expression can cause damage in living systems. While cells are usually well-equipped to modulate their own transcriptional behavior, an investigation into pathological gene expression indicates that many situations arise wherein the expected regulatory response fails. Our device is designed to augment endogenous gene regulatory pathways.</p> | ||
| - | <p>While one can surely identify numerous cases of abnormal gene expression in cellular systems, we turn our attention to one particular network related to a crucial decision in cell fate, apoptosis.</p> | + | <!-- |
| - | + | <p>While one can surely identify numerous cases of abnormal gene expression in cellular systems, we turn our attention to one particular network related to a crucial decision in cell fate, apoptosis.</p> | |
=Cellular suicide and the cancer phenotype= | =Cellular suicide and the cancer phenotype= | ||
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=Apoptosis in yeast= | =Apoptosis in yeast= | ||
| - | While still an ongoing debate, there is increasingly more evidence that yeast have apoptosis as well (Frohlich et al., 2007). Despite the fact that apoptosis seems to make most sense in a multicellular context, the organisms nonetheless show signs characteristic of a programmed cell death. In fact, much research about apoptotic pathways from mammals can be conducted in yeast, due to the fact that many of the genes and pathways present in mammals share homology to those found in yeast. Given this promising range of homology, one might consider first applying the regulatory approach discussed above for mammals in a yeast framework. A limiter device in yeast could also serve as a useful tool for understanding important nodes in the apoptotic network. | + | While still an ongoing debate, there is increasingly more evidence to suggest that yeast have apoptosis as well (Frohlich et al., 2007). Despite the fact that apoptosis seems to make most sense in a multicellular context, the organisms nonetheless show signs characteristic of a programmed cell death. In fact, much research about apoptotic pathways from mammals can be conducted in yeast, due to the fact that many of the genes and pathways present in mammals share homology to those found in yeast. Given this promising range of homology, one might consider first applying the regulatory approach discussed above for mammals in a yeast framework. A limiter device in yeast could also serve as a useful tool for understanding important nodes in the apoptotic network. |
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=References= | =References= | ||
| - | 1. Frohlich et al. Yeast apoptosis—From genes to pathways. ''Seminars in Cancer Biology'' 17 (2007) 112–121 | + | <br>1. Frohlich et al. Yeast apoptosis—From genes to pathways. ''Seminars in Cancer Biology'' 17 (2007) 112–121 |
| - | + | <br>2. Toledo and Wahl, Regulating the p53 pathway:in vitro hypotheses, in vivo veritas, ''Nature Reviews'' vol 6. 2006 | |
| - | + | <br>3. Vucic and Fairbrother, The Inhibitor of Apoptosis Proteins as Therapeutic Targets in Cancer, ''Clin Cancer Res.'' 2007;13(20) | |
| - | 2. Toledo and Wahl, Regulating the p53 pathway:in vitro hypotheses, in vivo veritas, ''Nature Reviews'' vol 6. 2006 | + | |
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Latest revision as of 16:34, 8 November 2010
The utility of threshold limitationMuch as excessive signal levels can destroy a radio transmitter, excessive genetic expression can cause damage in living systems. While cells are usually well-equipped to modulate their own transcriptional behavior, an investigation into pathological gene expression indicates that many situations arise wherein the expected regulatory response fails. Our device is designed to augment endogenous gene regulatory pathways.
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