| pubmed-article:14561707 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1705320 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C0071253 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1335202 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C0694894 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C0694895 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:14561707 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:14561707 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:14561707 | pubmed:dateCreated | 2003-10-16 | lld:pubmed |
| pubmed-article:14561707 | pubmed:abstractText | Tuberous sclerosis (TSC) is a familial tumor syndrome due to mutations in TSC1 or TSC2, in which progression to malignancy is rare. Primary Tsc2(-/-) murine embryo fibroblast cultures display early senescence with overexpression of p21CIP1/WAF1 that is rescued by loss of TP53. Tsc2(-/-)TP53(-/-) cells, as well as tumors from Tsc2(+/-) mice, display an mTOR-activation signature with constitutive activation of S6K, which is reverted by treatment with rapamycin. Rapamycin also reverts a growth advantage of Tsc2(-/-)TP53(-/-) cells. Tsc1/Tsc2 does not bind directly to mTOR, however, nor does it directly influence mTOR kinase activity or cellular phosphatase activity. There is a marked reduction in Akt activation in Tsc2(-/-)TP53(-/-) and Tsc1(-/-) cells in response to serum and PDGF, along with a reduction in cell ruffling. PDGFRalpha and PDGFRbeta expression is markedly reduced in both the cell lines and Tsc mouse renal cystadenomas, and ectopic expression of PDGFRbeta in Tsc2-null cells restores Akt phosphorylation in response to serum, PDGF, EGF, and insulin. This activation of mTOR along with downregulation of PDGFR PI3K-Akt signaling in cells lacking Tsc1 or Tsc2 may explain why these genes are rarely involved in human cancer. This is in contrast to PTEN, which is a negative upstream regulator of this pathway. | lld:pubmed |
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| pubmed-article:14561707 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:14561707 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:14561707 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14561707 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:14561707 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:KwiatkowskiDa... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:ZhangHongbing... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:OndaHiroakiH | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:CicchettiGreg... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:CarpenterChri... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:VazquezFranci... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:KoonHenry BHB | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:AsricanKirste... | lld:pubmed |
| pubmed-article:14561707 | pubmed:author | pubmed-author:BajraszewskiN... | lld:pubmed |
| pubmed-article:14561707 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14561707 | pubmed:volume | 112 | lld:pubmed |
| pubmed-article:14561707 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14561707 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14561707 | pubmed:pagination | 1223-33 | lld:pubmed |
| pubmed-article:14561707 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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