[IP] OK: latest research shows an anti-rejection drug (that is just being tested for as an anti-cancer agent) could protect kidneys.....
- To: <email @ redacted>
- Subject: [IP] OK: latest research shows an anti-rejection drug (that is just being tested for as an anti-cancer agent) could protect kidneys.....
- From: yerachmiel bruchya haLevi <email @ redacted>
- Date: Tue, 28 Jun 2011 11:36:37 -0400
- Reply-To: email @ redacted
According to the latest issue of the Journal of Clinical Investigation,
Professor Dr. Tobias Huber, a kidney expert at the Nephrology Division of
the University Medical Center Freiburg, Germany (a teaching hospital and
medical research unit of the University of Freiburg and well known for its
advanced research), along with the help of the Cluster of Excellence BIOSS
(Center for Biological Signaling Studies), and his team have been able to
make new discoveries as to why the kidneys fail as a result of diabetes.
This new research data was able to identify a signaling path that affects
the progression of kidney disease in diabetic patients. mTOR (which belongs
to the phosphatidylinositol 3-kinase-related kinase protein
99t-know-about-protein/> family) is a metabolic enzyme that controls the
growth and reproduction of cells. Through research, it has been shown that
diabetes, either Type 1 or Type 2, causes the mTOR signaling path to become
overactive. When the signaling path becomes overactive, it causes damage to
the kidney cells which in turn leads to kidney failure.
Basal activation of mTOR may be proven to be vital for the regular function
of renal corpuscles during human development, but the overactive mTOR can
result in breakdown of kidney filtering in diabetic patients, which
eventually leads to the total shutdown of the kidneys.
Using animals for testing, the researchers were able to stop the signaling
path and able to stop the kidney disease in its tracks. If applied to
diabetic patients with kidney failure in the future, this is a chance for
the end of kidney failure in those suffering from any form of diabetes.
The mammalian target of rapamycin (mTOR) also known as mechanistic target of
rapamycin or FK506 binding protein 12-rapamycin associated protein 1 (FRAP1)
is a <http://en.wikipedia.org/wiki/Protein> protein which in humans is
encoded by the FRAP1 <http://en.wikipedia.org/wiki/Gene> gene.
60990-1>  mTOR is a
serine/threonine protein kinase that regulates cell growth,
<http://en.wikipedia.org/wiki/Cell_proliferation> cell proliferation, cell
<http://en.wikipedia.org/wiki/Motility> motility, cell survival,
<http://en.wikipedia.org/wiki/Protein_synthesis> protein synthesis, and
s-3>  mTOR belongs to the
phosphatidylinositol 3-kinase-related kinase protein family
Current efforts in anticancer drug development are targeting key factors in
cell-cycle regulation. Mammalian target of rapamycin (mTOR) is one such
protein kinase that facilitates cell growth by stimulating the cell to
traverse the G1 to S phase of the cell cycle. Rapamycin is the first defined
inhibitor of mTOR, and the demonstration of its antitumor activity has led
to great interest in this pathway as an antitumor mechanism. Analogues with
better pharmacologic properties have been developed and have entered
clinical trials. Human cell lines of renal cell cancer, among several other
tumors, are sensitive to growth inhibition via this pathway. Ongoing
clinical trials are evaluating renal cell cancer and other malignancies
using therapy with mTOR inhibitors. These agents are more likely to induce
growth inhibition rather than tumor regression
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