In this world of infections, Ciprofloxacin has gained prominent place and is widely prescribed and many antibiotics have similar effect of immunomodulation on mainly the monocytes and of course the lymphocytes. Widespread use of these antibiotics call for further discrimination at genetic levels. Ciprofloxacin has been known to amplify several genes including the NFKB, JUN B, C-Myc, AP-1, NFAT, c-fos, c-JUN, fra-1. The NFAT amplification has the most of the attention here...This amplification calls for a check on the GSK3B because a secondary amplification of this gene hits many critical genes in the initiation of cancers! And in a profoundly obese population, the GSK3B has to be assumed to be profoundly disturbed in terms of level. A high amplification of this gene not only affect key genes but is associated with marked phosphorylation of other genes particularly when interacting with SGK3. And phosporylation of genes has been implicated in the expansion neoplastic transformations. i.e the story of Casein Receptors and their relation with breast cancers.
Concurrent amplification of NFAT and GSK3 may be dangerous
1.when interacting with AR- --(Androgen Receptors) because Prostate Cancer may result
2.MUC 1, because Colon cancer may result
3.P53 and the Catenin, the NOTCH, all implicated in various cancers (Breast,tuberous etc..)
Do we check the status of this gene? no, we are still waiting for clinical trials...can't wait to live in the next century when all this will be done! don't take my words for them!
WIKIPEDIA :
GSK3B has been shown to
interact with:
- AKAP11,[6]
- AXIN1,[7][8]
- AXIN2,[9][10]
- AR,[11]
- CTNNB1,[12][13]
- DNM1L,[14]
- MACF1[15]
- MUC1,[16][17]
- SMAD3[18]
- NOTCH1,[19]
- NOTCH2,[20]
- P53,[21]
- PRKAR2A,[6]
- SGK3,[22] and
- TSC2.[7][23]
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- " Nuclear import of NFAT proteins is opposed by maintenance kinases in the
cytoplasm and export kinases in the nucleus. Export kinases, such as PKA and GSK-3β, must be inactivated for NFAT nuclear retention."
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