Rosis complex 2 Most of the evidence to date, however, has another substrate of Akt, the mammalian target of rapamycin, such as the R The most important in tumorigenesis. mTOR is a serine / threonine kinase that plays a role Critics in the regulation of cell growth, survival, motility and division of t. mTOR acts through mTORC1 and mTORC2 two different complexes.

WZ8040 Each consists of mTOR is associated with LST8 and Raptor Education mTORC1 mTORC2 or Rictor training. When activated, increases the mRNA translation by ht mTORC1 phosphorylation of downstream molecules of p70 S6K and 4E binding protein first S6K phosphorylates S6 part of the 40S ribosomal subunit, the translation of mRNA more and more. 4E BP1 phosphorylation leads to activation of the translation, but prevents the association of 4E BP1 with the eukaryotic initiation factor 4F complex.
mTORC2 functions are less well understood. Completely has recently been shown that mTORC2 be involved in Akt phosphorylation at Ser473, which is, by phosphorylation at Thr308 by PDK1 for Requests reference requests getting activation of Akt is required. The most important negative regulator of the PI3K/Akt/mTOR the tumor suppressor phosphatase and tensin homolog on BIIB021 HSP-90 inhibitor chromosome 10 gel Deleted. This phosphatase on the position D3 PIP3 is phosphorylated, f Promotes the formation of PIP2 and directly against the action of PI3K. PTEN plays a role Crucial role in the contr The Gr E of the cell, organ size E and proliferation, and loss of PTEN is the hour For a common cause of activation of the PI3K signaling pathway in human cancers.
ACTIVITY ITMN-191 PI3K/Akt/mTOR Ver Changes in prostate cancer were detected in prostate tissue PI3K/Akt/mTOR in several studies, suggesting that this pathway plays a role The market leader in the development and progression of prostate cancer. It is business Protected, that up-regulation occurs at 30 to 50% of prostate cancer, and aberrant signaling molecules in this pathway is also detected in prostate cancer cell lines and xenografts. PTEN is a negative regulator of the activity T of the PI3K/Akt/mTOR path. PTEN deletions and mutations that lead to expression of inactive protein to an increased Hten activity T of the PI3K/Akt/mTOR path. Mutations in the PTEN tumor suppressor gene are h INDICATIVE events in prostate cancer, with studies showing loss of heterozygosity at the PTEN locus in 60% of the samples from prostate cancer.
Reduced expression of PTEN was found in 85% of the prime Ren tumors compared to normal tissue from the same patients, and PTEN expression was also reduced in relative numbers of cancer of prostatic intraepithelial neoplasia. Ver changes In the expression of PTEN are a number of variables in the pathologic prostate cancer. The loss of PTEN expression with Gleason score and pathological stage of the primary Rtumors and h Higher incidence of lymph node metastases correlated development. If, in addition to the detection of phospho Akt were combined, PTEN status was the primary Rtumors a better predictor of PSA recurrence of phospho act alone. Importantly, had 90% of patients with primary Ren PTEN negative tumors do not occur with high phospho Akt, a biochemical recurrence, w While 88% of tumors with low positive PTEN phosphorylated Akt in the study period. In vitro and pr Clinical studies have also shown that inactivation of PTEN leads to Con