| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| A Nakashio, N Fujita, S Rokudai, S Sato, T Tsuru. Prevention of phosphatidylinositol 3'-kinase-Akt survival signaling pathway during topotecan-induced apoptosis. Cancer research. vol 60. issue 18. 2000-10-13. PMID:11016662. |
the serine/threonine kinase akt (also known as protein kinase b) is a downstream effector of phosphatidylinositol-3'-kinase [pi(3)k] that is recognized as the major mediator of survival signals that protect cells from undergoing apoptosis. |
2000-10-13 |
2023-08-12 |
human |
| Y Kureishi, Z Luo, I Shiojima, A Bialik, D Fulton, D J Lefer, W C Sessa, K Wals. The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals. Nature medicine. vol 6. issue 9. 2000-10-06. PMID:10973320. |
accordingly, simvastatin enhanced phosphorylation of the endogenous akt substrate endothelial nitric oxide synthase (enos), inhibited apoptosis and accelerated vascular structure formation in vitro in an akt-dependent manner. |
2000-10-06 |
2023-08-12 |
Not clear |
| N L Ge, S Rudikof. Expression of PTEN in PTEN-deficient multiple myeloma cells abolishes tumor growth in vivo. Oncogene. vol 19. issue 36. 2000-10-02. PMID:10962569. |
in myeloma cells, pip's are required for phosphorylation of akt, a key event leading to inhibition of apoptosis. |
2000-10-02 |
2023-08-12 |
mouse |
| N L Ge, S Rudikof. Expression of PTEN in PTEN-deficient multiple myeloma cells abolishes tumor growth in vivo. Oncogene. vol 19. issue 36. 2000-10-02. PMID:10962569. |
ectopic expression of wild type pten in opm-2 cells inhibited akt phosphorylation which was correlated with an increase in apoptosis. |
2000-10-02 |
2023-08-12 |
mouse |
| M Sibilia, A Fleischmann, A Behrens, L Stingl, J Carroll, F M Watt, J Schlessinger, E F Wagne. The EGF receptor provides an essential survival signal for SOS-dependent skin tumor development. Cell. vol 102. issue 2. 2000-09-14. PMID:10943841. |
the k5-sos-f papillomas and primary keratinocytesfrom wa2 mice display increased apoptosis, reduced akt phosphorylation and grafting experiments imply a cell-autonomous requirement for egfr in keratinocytes. |
2000-09-14 |
2023-08-12 |
mouse |
| J Verdu, M A Buratovich, E L Wilder, M J Birnbau. Cell-autonomous regulation of cell and organ growth in Drosophila by Akt/PKB. Nature cell biology. vol 1. issue 8. 2000-09-08. PMID:10587646. |
ectopic expression of akt does not affect cell-fate determination, apoptosis or proliferation rates in imaginal discs. |
2000-09-08 |
2023-08-12 |
drosophila_melanogaster |
| Y Hu, L Qiao, S Wang, S B Rong, E J Meuillet, M Berggren, A Gallegos, G Powis, A P Kozikowsk. 3-(Hydroxymethyl)-bearing phosphatidylinositol ether lipid analogues and carbonate surrogates block PI3-K, Akt, and cancer cell growth. Journal of medicinal chemistry. vol 43. issue 16. 2000-09-08. PMID:10956212. |
akt inhibits apoptosis by phosphorylating bad, thus promoting its binding to and blockade of the activity of the cell survival factor bcl-x. |
2000-09-08 |
2023-08-12 |
Not clear |
| Y Kashii, M Uchida, K Kirito, M Tanaka, K Nishijima, M Toshima, T Ando, K Koizumi, T Endoh, K Sawada, M Momoi, Y Miura, K Ozawa, N Komats. A member of Forkhead family transcription factor, FKHRL1, is one of the downstream molecules of phosphatidylinositol 3-kinase-Akt activation pathway in erythropoietin signal transduction. Blood. vol 96. issue 3. 2000-08-24. PMID:10910908. |
in addition, overexpression of the constitutively active form of akt on ut-7/epo cells partially blocked apoptosis induced by withdrawal of epo from the culture medium. |
2000-08-24 |
2023-08-12 |
human |
| S L Pogue, T Kurosaki, J Bolen, R Herbs. B cell antigen receptor-induced activation of Akt promotes B cell survival and is dependent on Syk kinase. Journal of immunology (Baltimore, Md. : 1950). vol 165. issue 3. 2000-08-22. PMID:10903730. |
while parental dt40 cells undergo apoptosis in response to bcr cross-linking, cells overexpressing akt show a greatly diminished apoptotic response. |
2000-08-22 |
2023-08-12 |
chicken |
| C A Jamieson, K R Yamamot. Crosstalk pathway for inhibition of glucocorticoid-induced apoptosis by T cell receptor signaling. Proceedings of the National Academy of Sciences of the United States of America. vol 97. issue 13. 2000-07-31. PMID:10860997. |
in contrast, phosphatidylinositol 3-kinase and akt, which down-regulate other lymphocyte apoptosis pathways, did not inhibit glucocorticoid-induced apoptosis. |
2000-07-31 |
2023-08-12 |
Not clear |
| Z Chen, J Sun, A Pradines, G Favre, J Adnane, S M Sebt. Both farnesylated and geranylgeranylated RhoB inhibit malignant transformation and suppress human tumor growth in nude mice. The Journal of biological chemistry. vol 275. issue 24. 2000-07-20. PMID:10770919. |
here we demonstrate that both rhob-f and rhob-gg inhibit anchorage-dependent and -independent growth, induce apoptosis, inhibit constitutive activation of erk and insulin-like growth factor-1 stimulation of akt, and suppress tumor growth in nude mice. |
2000-07-20 |
2023-08-12 |
mouse |
| K Kinoshita, D R Taupin, H Itoh, D K Podolsk. Distinct pathways of cell migration and antiapoptotic response to epithelial injury: structure-function analysis of human intestinal trefoil factor. Molecular and cellular biology. vol 20. issue 13. 2000-07-20. PMID:10848594. |
the inability to block apoptosis correlated with a loss of trefoil peptide-induced transactivation of the egf receptor or akt kinase in ht-29 cells. |
2000-07-20 |
2023-08-12 |
human |
| D K Podolsk. Mechanisms of regulatory peptide action in the gastrointestinal tract: trefoil peptides. Journal of gastroenterology. vol 35 Suppl 12. 2000-06-28. PMID:10779222. |
among other effects, activation of these pathways is associated with redistribution of e-cadherin from the cell surface to intracellular domains, where it is complexed with catenins, and phosphorylation of akt, inactivating this kinase associated with apoptosis. |
2000-06-28 |
2023-08-12 |
Not clear |
| P Maroni, P Bendinelli, C Zuccorononno, L Schiaffonati, R Piccolett. Cellular signalling after in vivo heat shock in the liver. Cell biology international. vol 24. issue 3. 2000-06-26. PMID:10772775. |
gsk3, which may act downstream to pi3-kinase through akt, undergoes hyperphosphorylation, thus playing a possible role in the protection from apoptosis and in the modulation of heat-shock transcription factor activity. |
2000-06-26 |
2023-08-12 |
rat |
| J W Davis, K Melendez, V M Salas, F T Lauer, S W Burchie. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibits growth factor withdrawal-induced apoptosis in the human mammary epithelial cell line, MCF-10A. Carcinogenesis. vol 21. issue 5. 2000-06-15. PMID:10783307. |
since tcdd stimulates pi3k activity, the phosphorylation status of akt, a serine/threonine kinase that mediates pi3k-dependent inhibition of apoptosis, was examined. |
2000-06-15 |
2023-08-12 |
human |
| M E Burow, C B Weldon, L I Melnik, B N Duong, B M Collins-Burow, B S Beckman, J A McLachla. PI3-K/AKT regulation of NF-kappaB signaling events in suppression of TNF-induced apoptosis. Biochemical and biophysical research communications. vol 271. issue 2. 2000-06-13. PMID:10799299. |
we found that in mcf-7 breast carcinoma cells, pi3k and akt suppressed a dose-dependent induction of apoptosis by tumor necrosis factor alpha (tnf). |
2000-06-13 |
2023-08-12 |
Not clear |
| M E Burow, C B Weldon, L I Melnik, B N Duong, B M Collins-Burow, B S Beckman, J A McLachla. PI3-K/AKT regulation of NF-kappaB signaling events in suppression of TNF-induced apoptosis. Biochemical and biophysical research communications. vol 271. issue 2. 2000-06-13. PMID:10799299. |
pi3k-akt signaling activated nf-kappab through both tnfr signaling-dependent and -independent mechanisms, potentially representing a mechanism by which akt functions to suppress apoptosis in cancer. |
2000-06-13 |
2023-08-12 |
Not clear |
| X Wang, K D McCullough, T F Franke, N J Holbroo. Epidermal growth factor receptor-dependent Akt activation by oxidative stress enhances cell survival. The Journal of biological chemistry. vol 275. issue 19. 2000-06-08. PMID:10799549. |
akt provides a survival signal that protects cells from apoptosis induced by growth factor withdrawal, but its function in other forms of stress is less clear. |
2000-06-08 |
2023-08-12 |
Not clear |
| X Wang, K D McCullough, T F Franke, N J Holbroo. Epidermal growth factor receptor-dependent Akt activation by oxidative stress enhances cell survival. The Journal of biological chemistry. vol 275. issue 19. 2000-06-08. PMID:10799549. |
wortmannin and ly294002 treatment significantly enhanced h(2)o(2)-induced apoptosis, whereas expression of exogenous myristoylated akt (an activated form) inhibited cell death. |
2000-06-08 |
2023-08-12 |
Not clear |
| X Wang, K D McCullough, T F Franke, N J Holbroo. Epidermal growth factor receptor-dependent Akt activation by oxidative stress enhances cell survival. The Journal of biological chemistry. vol 275. issue 19. 2000-06-08. PMID:10799549. |
these results suggest that h(2)o(2) activates akt via an egfr/pi3-k-dependent pathway and that elevated akt activity confers protection against oxidative stress-induced apoptosis. |
2000-06-08 |
2023-08-12 |
Not clear |