MEK, ERK and PI3K Akt mTOR PTEN signaling
pathways. These pathways exert their effects on p53 itself, and signal transduction inhibitors of cell proliferation and inhibit AS-604850 aging can k. Anything similar effects on the pr Prevention of cellular Ren Senescence were with resveratrol, the active ingredient in the skin of red grapes, has been shown, mTOR and p70S6K as cellular Re inhibit senescence observed contained. Other studies have shown that metformin diabetes drug h Frequently prescribed also inhibits mTOR and prevent cell aging. must be adjusted as the Ras-Raf MEK and ERK AKT signaling pathways Ras PI3K PTEN mTOR interact to the activity of t of mTOR and downstream components of this pathway for mRNA stability t and protein translation of both genes involved in essential growth and survival critically , is gesch proof, that by blocking some of the main roads, it can m be possible to prevent cell aging.
Conclusions Several pharmaceutical companies have developed inhibitors of the Ras Raf MEK ERK. At the beginning of the MEK inhibitors proved the h HIGHEST specificity t have. But k Can these inhibitors limited effectiveness in the treatment of cancer in humans have, unless the particular cancer proliferates CX-5461 in direct response to the Raf MEK ERK. Furthermore, MEK inhibitors h Frequently cytostatics pleased t as cytotoxic and thus their F Ability to function as effective tools in the fight against cancer as a single agent is limited, and they can be more effective if or chemotherapy in combination with radiotherapy.
Raf inhibitors have also been developed, and some are for the treatment of patients to be treated with different types of cancer. This particular Raf inhibitor inhibits also other receptors and kinases, which are necessary for the growth of cancer can be, in particular. The promiscuous nature sorafenib has helped the effectiveness of this particular Raf inhibitor of certain cancers. Specific mutants Raf and PI3K inhibitors are also being developed. This is perhaps the most exciting area in terms of development of inhibitors because they have entered dinner mutated gene targeting to rdern the proliferation of tumor-specific f. However, problems with some inhibitors of Raf mutant allele B were identified as resulting in activation of Raf-1 is also when Ras is mutated.
A combined treatment with drugs or physical or other traditional inhibitor, a specific molecule in a signal transduction pathway is directed otherwise is an essential step in order to improve the effectiveness and usefulness of Raf and MEK inhibitors. Rapamycins updated, rapalogs used to treat patients with cancer different W While rapalogs are effective and their toxicity T profiles are known, a inh Pension property that they are not very cytotoxic when it comes to tumor cells abzut How it is This inh Pension property of rapamycin may also their low toxicity T help humans. Mutations in several genes entered upstream receptors or Ras dinner Raf MEK ERK anomalies PI3K and PTEN activation of Akt mTOR pathway. Where the targeting of these components in cascade with low molecular weight inhibitors can inhibit cell growth. K the usefulness of these inhibitors can have on the mechanism of transformation of cancer nts especially dependent. If the tumor has a dependence Dependence Ras Raf MEK ERK signaling pathway, then it may be sensitive to Raf M