Difference between revisions of "Part:BBa K729001"
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===Description=== | ===Description=== | ||
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| + | The protein IrrE originates from Deinococcus radiodurans, where it confers resistance to radiation. When transformed into E. Coli however, it protected against salt, oxidative and thermal shock. IrrE appears to function as a global regulator of stress factor genes. So far it has been demonstrated to upregulate transcription of recA and pprA – genes which encode Recombinase A and Radiation Inducible Protein. With respect to salt tolerance, IrrE upregulates the production of several stress responsive proteins, protein kinases, metabolic proteins, and detoxification proteins. It also downregulates glycerol degradation. With this global regulatory effect, E. Coli becomes more salt tolerant. | ||
===Characterisation=== | ===Characterisation=== | ||
Revision as of 22:38, 16 September 2012
irrE from Deinococcus radiodurans
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
Description
The protein IrrE originates from Deinococcus radiodurans, where it confers resistance to radiation. When transformed into E. Coli however, it protected against salt, oxidative and thermal shock. IrrE appears to function as a global regulator of stress factor genes. So far it has been demonstrated to upregulate transcription of recA and pprA – genes which encode Recombinase A and Radiation Inducible Protein. With respect to salt tolerance, IrrE upregulates the production of several stress responsive proteins, protein kinases, metabolic proteins, and detoxification proteins. It also downregulates glycerol degradation. With this global regulatory effect, E. Coli becomes more salt tolerant.