-
2
-
-
0028328655
-
Rapamycin selectively inhibits the growth of childhood rhabdomyosarcoma cells through inhibition of signaling via the type I insulin-like growth factor receptor
-
Dilling MB, Dias P, Shapiro DN, Germain GS, Johnson RK, Houghton PJ. Rapamycin selectively inhibits the growth of childhood rhabdomyosarcoma cells through inhibition of signaling via the type I insulin-like growth factor receptor. Cancer Res. 54:1994;903-907.
-
(1994)
Cancer Res
, vol.54
, pp. 903-907
-
-
Dilling, M.B.1
Dias, P.2
Shapiro, D.N.3
Germain, G.S.4
Johnson, R.K.5
Houghton, P.J.6
-
3
-
-
0028925744
-
Rapamycin enhances apoptosis and increases sensitivity to cisplatin in vitro
-
Shi Y, Frankel A, Radvanyi LG, Penn LZ, Miller RG, Mills GB. Rapamycin enhances apoptosis and increases sensitivity to cisplatin in vitro. Cancer Res. 55:1995;1982-1988.
-
(1995)
Cancer Res
, vol.55
, pp. 1982-1988
-
-
Shi, Y.1
Frankel, A.2
Radvanyi, L.G.3
Penn, L.Z.4
Miller, R.G.5
Mills, G.B.6
-
4
-
-
0029794614
-
Rapamycin inhibits constitutive p70s6k phosphorylation, cell proliferation, and colony formation in small cell lung cancer cells
-
Seufferlein T, Rozengurt E. Rapamycin inhibits constitutive p70s6k phosphorylation, cell proliferation, and colony formation in small cell lung cancer cells. Cancer Res. 56:1996;3895-3897.
-
(1996)
Cancer Res
, vol.56
, pp. 3895-3897
-
-
Seufferlein, T.1
Rozengurt, E.2
-
5
-
-
0028950217
-
Isolation of a protein target of the FKBP12-rapamycin complex in mammalian cells
-
Sabers CJ, Martin MM, Brunn GJ, Williams JM, Dumont FJ, Wiederrecht G, Abraham RT. Isolation of a protein target of the FKBP12-rapamycin complex in mammalian cells. J Biol Chem. 270:1995;815-822.
-
(1995)
J Biol Chem
, vol.270
, pp. 815-822
-
-
Sabers, C.J.1
Martin, M.M.2
Brunn, G.J.3
Williams, J.M.4
Dumont, F.J.5
Wiederrecht, G.6
Abraham, R.T.7
-
6
-
-
0028360374
-
A mammalian protein targeted by G1-arresting rapamycin-receptor complex
-
Brown EJ, Albers MW, Shin TB, Ichikawa K, Keith CT, Lane WS, Schreiber SL. A mammalian protein targeted by G1-arresting rapamycin-receptor complex. Nature. 369:1994;756-758.
-
(1994)
Nature
, vol.369
, pp. 756-758
-
-
Brown, E.J.1
Albers, M.W.2
Shin, T.B.3
Ichikawa, K.4
Keith, C.T.5
Lane, W.S.6
Schreiber, S.L.7
-
7
-
-
0028239893
-
RAFT1: A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs
-
Sabatini DM, Erdjument-Bromage H, Liu M, Tempst P, Snyder SH. RAFT1: A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs. Cell. 78:1994;35-43.
-
(1994)
Cell
, vol.78
, pp. 35-43
-
-
Sabatini, D.M.1
Erdjument-Bromage, H.2
Liu, M.3
Tempst, P.4
Snyder, S.H.5
-
8
-
-
0028598672
-
RAPT1, a mammalian homolog of yeast Tor, interacts with the FKBP12/rapamycin complex
-
Chiu MI, Katz H, Berlin V. RAPT1, a mammalian homolog of yeast Tor, interacts with the FKBP12/rapamycin complex. Proc Natl Acad Sci USA. 91:1994;12574-12578.
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 12574-12578
-
-
Chiu, M.I.1
Katz, H.2
Berlin, V.3
-
9
-
-
0025776523
-
Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast
-
Heitman J, Movva NR, Hall MN. Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast. Science. 253:1991;905-909.
-
(1991)
Science
, vol.253
, pp. 905-909
-
-
Heitman, J.1
Movva, N.R.2
Hall, M.N.3
-
11
-
-
0027382875
-
Dominant missense mutations in a novel yeast protein related to mammalian phosphatidylinositol 3-kinase and VPS34 abrogate rapamycin cytotoxicity
-
Cafferkey R, Young PR, McLaughlin MM, Bergsma DJ, Koltin Y, Sathe GM, Faucette L, Eng W-K, Johnson RK, Livi GP. Dominant missense mutations in a novel yeast protein related to mammalian phosphatidylinositol 3-kinase and VPS34 abrogate rapamycin cytotoxicity. Mol Cell Biol. 13:1993;6012-6023.
-
(1993)
Mol Cell Biol
, vol.13
, pp. 6012-6023
-
-
Cafferkey, R.1
Young, P.R.2
McLaughlin, M.M.3
Bergsma, D.J.4
Koltin, Y.5
Sathe, G.M.6
Faucette, L.7
Eng W-K8
Johnson, R.K.9
Livi, G.P.10
-
12
-
-
0028137771
-
TOR1 and TOR2 are structurally and functionally similar but not identical phosphatidylinositol kinase homologues in yeast
-
Helliwell SB, Wagner P, Kunz J, Dueter-Reinhard M, Henriquez R, Hall MN. TOR1 and TOR2 are structurally and functionally similar but not identical phosphatidylinositol kinase homologues in yeast. Mol Biol. 5:1994;105-118.
-
(1994)
Mol Biol
, vol.5
, pp. 105-118
-
-
Helliwell, S.B.1
Wagner, P.2
Kunz, J.3
Dueter-Reinhard, M.4
Henriquez, R.5
Hall, M.N.6
-
13
-
-
0030479340
-
TOR2 is required for organization of the actin cytoskeleton in yeast
-
Schmidt A, Kunz J, Hall MN. TOR2 is required for organization of the actin cytoskeleton in yeast. Proc Natl Acad Sci USA. 93:1996;13780-13785.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 13780-13785
-
-
Schmidt, A.1
Kunz, J.2
Hall, M.N.3
-
14
-
-
0028856331
-
When is a lipid kinase not a lipid kinase? When it is a protein kinase
-
Hunter T. When is a lipid kinase not a lipid kinase? When it is a protein kinase. Cell. 83:1995;1-4.
-
(1995)
Cell
, vol.83
, pp. 1-4
-
-
Hunter, T.1
-
15
-
-
0028800996
-
PIK-related kinases: DNA repair, recombination, and cell cycle checkpoints
-
Keith CT, Schreiber SL. PIK-related kinases: DNA repair, recombination, and cell cycle checkpoints. Science. 270:1995;50-51.
-
(1995)
Science
, vol.270
, pp. 50-51
-
-
Keith, C.T.1
Schreiber, S.L.2
-
17
-
-
0031472044
-
Cell-cycle signaling: Atm displays its many talents
-
Westphal CH. Cell-cycle signaling: Atm displays its many talents. Curr Biol. 7:1997;R789-R792.
-
(1997)
Curr Biol
, vol.7
-
-
Westphal, C.H.1
-
18
-
-
0030879563
-
Atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity
-
of special interest. This paper addresses the long-suspected possibility that the ataxia telangiectasia mediated (ATM) kinase and the tumor suppressor protein p53 interact in the regulation of cellular responses to DNA damage. Focusing on thymocytes, the authors show that the functions of ATM and p53 in lymphogenesis and radiation toxicity are partially overlapping, but are clearly not completely congruent.
-
Westphal CH, Rowan S, Schmaltz C, Elson A, Fisher DE, Leder P. Atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity. of special interest Nature Genet. 16:1997;397-401 This paper addresses the long-suspected possibility that the ataxia telangiectasia mediated (ATM) kinase and the tumor suppressor protein p53 interact in the regulation of cellular responses to DNA damage. Focusing on thymocytes, the authors show that the functions of ATM and p53 in lymphogenesis and radiation toxicity are partially overlapping, but are clearly not completely congruent.
-
(1997)
Nature Genet
, vol.16
, pp. 397-401
-
-
Westphal, C.H.1
Rowan, S.2
Schmaltz, C.3
Elson, A.4
Fisher, D.E.5
Leder, P.6
-
19
-
-
0029103330
-
Control of p70 S6 kinase by the kinase activity FRAP in vivo
-
Brown EJ, Beal PA, Keith CT, Chen J, Shin TB, Schreiber SL. Control of p70 S6 kinase by the kinase activity FRAP in vivo. Nature. 377:1995;441-446.
-
(1995)
Nature
, vol.377
, pp. 441-446
-
-
Brown, E.J.1
Beal, P.A.2
Keith, C.T.3
Chen, J.4
Shin, T.B.5
Schreiber, S.L.6
-
20
-
-
0003018665
-
Ribosomal protein S6 phosphorylation and signal transduction
-
J.W.B. Hershey, M.B. Mathews, Sonenberg N. New York: Cold Spring Harbor Laboratory Press. Chapter 14
-
Jefferies HBJ, Thomas G. Ribosomal protein S6 phosphorylation and signal transduction. Hershey JWB, Mathews MB, Sonenberg N. Translational Control. 1996;389-409 Cold Spring Harbor Laboratory Press, New York. Chapter 14.
-
(1996)
Translational Control
, pp. 389-409
-
-
Jefferies, H.B.J.1
Thomas, G.2
-
21
-
-
0029828590
-
s6k phosphorylation sites, T-229 and T-389, are differentially regulated by rapamycin-insensitive kinase kinases
-
s6k phosphorylation sites, T-229 and T-389, are differentially regulated by rapamycin-insensitive kinase kinases. Mol Cell Biol. 16:1996;6242-6251.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 6242-6251
-
-
Dennis, P.B.1
Pullen, N.2
Kozma, S.C.3
Thomas, G.4
-
22
-
-
0032518467
-
3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase in vivo and in vitro
-
S6K, but also defines PDK1 as a multifunctional effector of PI3K-dependent signals in mammalian cells.
-
S6K, but also defines PDK1 as a multifunctional effector of PI3K-dependent signals in mammalian cells.
-
(1997)
Curr Biol
, vol.8
, pp. 69-81
-
-
Alessi, D.R.1
Kozlowski, M.T.2
Weng Q-P3
Morrice, N.4
Avruch, J.5
-
24
-
-
0030883848
-
PHAS/4E-BPs as regulators of mRNA translation and cell proliferation
-
Lawrence JC Jr, Abraham RT. PHAS/4E-BPs as regulators of mRNA translation and cell proliferation. Trends Biochem Sci. 22:1997;345-349.
-
(1997)
Trends Biochem Sci
, vol.22
, pp. 345-349
-
-
Lawrence J.C., Jr.1
Abraham, R.T.2
-
25
-
-
0030598885
-
A signaling pathway to translational control
-
Brown EJ, Schreiber SL. A signaling pathway to translational control. Cell. 86:1996;517-520.
-
(1996)
Cell
, vol.86
, pp. 517-520
-
-
Brown, E.J.1
Schreiber, S.L.2
-
26
-
-
0029968705
-
Initiation of protein synthesis in eukaryotic cells
-
Pain VM. Initiation of protein synthesis in eukaryotic cells. Eur J Biochem. 236:1996;747-771.
-
(1996)
Eur J Biochem
, vol.236
, pp. 747-771
-
-
Pain, V.M.1
-
27
-
-
0000831271
-
MRNA 5′ Cap-binding protein eIF4E and control of cell growth
-
J.W.B. Hershey, M.B. Mathews, Sonenberg N. New York: Cold Spring Harbor Laboratory Press. Chapter 8
-
Sonenberg N. mRNA 5′ Cap-binding protein eIF4E and control of cell growth. Hershey JWB, Mathews MB, Sonenberg N. Translational Control. 1996;245-269 Cold Spring Harbor Laboratory Press, New York. Chapter 8.
-
(1996)
Translational Control
, pp. 245-269
-
-
Sonenberg, N.1
-
28
-
-
0030949304
-
Translational controls impinging on the 5′-untranslated region and initiation factor proteins
-
Jackson RJ, Wickens M. Translational controls impinging on the 5′-untranslated region and initiation factor proteins. Curr Opin Genet Dev. 7:1997;233-241.
-
(1997)
Curr Opin Genet Dev
, vol.7
, pp. 233-241
-
-
Jackson, R.J.1
Wickens, M.2
-
29
-
-
0027365517
-
Elevated levels of cyclin D1 protein in response to increased expression of eukaryotic initiation factor 4E
-
Rosenwald IB, Lazaris-Karatzas A, Sonenberg N, Schmidt EV. Elevated levels of cyclin D1 protein in response to increased expression of eukaryotic initiation factor 4E. Mol Cell Biol. 13:1993;7358-7363.
-
(1993)
Mol Cell Biol
, vol.13
, pp. 7358-7363
-
-
Rosenwald, I.B.1
Lazaris-Karatzas, A.2
Sonenberg, N.3
Schmidt, E.V.4
-
30
-
-
0029166967
-
Eukaryotic translation initiation factor 4E regulates expression of cyclin D1 at transcriptional and post-transcriptional levels
-
Rosenwald IB, Kaspar R, Rousseau D, Gehrke L, Leboulch P, Chen J-J, Schmidt EV, Sonenberg N, London IM. Eukaryotic translation initiation factor 4E regulates expression of cyclin D1 at transcriptional and post-transcriptional levels. J Biol Chem. 270:1995;21176-21180.
-
(1995)
J Biol Chem
, vol.270
, pp. 21176-21180
-
-
Rosenwald, I.B.1
Kaspar, R.2
Rousseau, D.3
Gehrke, L.4
Leboulch, P.5
Chen J-J6
Schmidt, E.V.7
Sonenberg, N.8
London, I.M.9
-
31
-
-
0030041884
-
Translational initiation of ornithine decarboxylase and nucleocytoplasmic transport of cyclin D1 mRNA are increased in cells overexpressing eukaryotic initiation factor 4E
-
Rousseau D, Kaspar R, Rosenwald I, Gehrke L, Sonenberg N. Translational initiation of ornithine decarboxylase and nucleocytoplasmic transport of cyclin D1 mRNA are increased in cells overexpressing eukaryotic initiation factor 4E. Proc Natl Acad Sci USA. 93:1996;1065-1070.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 1065-1070
-
-
Rousseau, D.1
Kaspar, R.2
Rosenwald, I.3
Gehrke, L.4
Sonenberg, N.5
-
32
-
-
0025133071
-
Translation initiation factors induce DNA synthesis and transform NIH 3T3 cells
-
Smith MR, Jaramillo M, Liu Y-L, Dever TE, Merrick WC, Kung H-F, Sonenberg N. Translation initiation factors induce DNA synthesis and transform NIH 3T3 cells. New Biol. 2:1990;648-654.
-
(1990)
New Biol
, vol.2
, pp. 648-654
-
-
Smith, M.R.1
Jaramillo, M.2
Liu Y-L3
Dever, T.E.4
Merrick, W.C.5
Kung H-F6
Sonenberg, N.7
-
33
-
-
0026784679
-
Ras mediates translation initiation factor 4E-induced malignant transformation
-
Lazaris-Karatzas A, Smith MR, Frederickson RM, Jaramillo ML, Liu Y-L, Kung H-F, Sonenberg N. Ras mediates translation initiation factor 4E-induced malignant transformation. Genes Dev. 6:1992;1631-1642.
-
(1992)
Genes Dev
, vol.6
, pp. 1631-1642
-
-
Lazaris-Karatzas, A.1
Smith, M.R.2
Frederickson, R.M.3
Jaramillo, M.L.4
Liu Y-L5
Kung H-F6
Sonenberg, N.7
-
34
-
-
0030443685
-
The eIF4E-binding proteins 1 and 2 are negative regulators of cell growth
-
Rousseau D, Gingras A-C, Pause A, Sonenberg N. The eIF4E-binding proteins 1 and 2 are negative regulators of cell growth. Oncogene. 13:1996;2415-2420.
-
(1996)
Oncogene
, vol.13
, pp. 2415-2420
-
-
Rousseau, D.1
Gingras A-C2
Pause, A.3
Sonenberg, N.4
-
35
-
-
0029095931
-
Control of PHAS-I by insulin in 3T3-L1 adipocytes
-
Lin T-A, Kong X, Saltiel AR, Blackshear PJ, Lawrence JC Jr. Control of PHAS-I by insulin in 3T3-L1 adipocytes. J Biol Chem. 270:1995;18531-18538.
-
(1995)
J Biol Chem
, vol.270
, pp. 18531-18538
-
-
Lin T-A1
Kong, X.2
Saltiel, A.R.3
Blackshear, P.J.4
Lawrence J.C., Jr.5
-
36
-
-
0029120591
-
CAMP- And rapamycin-sensitive regulation of the association of eukaryotic initiation factor 4E and the translational regulator PHAS-I in aortic smooth muscle cells
-
Graves LM, Bornfeldt KE, Argast GM, Krebs EG, Kong X, Lin TA, Lawrence JC Jr. cAMP- and rapamycin-sensitive regulation of the association of eukaryotic initiation factor 4E and the translational regulator PHAS-I in aortic smooth muscle cells. Proc Natl Acad Sci USA. 92:1995;7222-7226.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 7222-7226
-
-
Graves, L.M.1
Bornfeldt, K.E.2
Argast, G.M.3
Krebs, E.G.4
Kong, X.5
Lin, T.A.6
Lawrence J.C., Jr.7
-
38
-
-
0029831167
-
Direct inhibition of the signaling functions of the mammalian target of rapamycin by the phosphoinositide 3-kinase inhibitors, wortmannin and LY294002
-
Brunn GJ, Williams J, Sabers C, Wiederrecht G, Lawrence JC Jr, Abraham RT. Direct inhibition of the signaling functions of the mammalian target of rapamycin by the phosphoinositide 3-kinase inhibitors, wortmannin and LY294002. EMBO J. 15:1996;5256-5267.
-
(1996)
EMBO J
, vol.15
, pp. 5256-5267
-
-
Brunn, G.J.1
Williams, J.2
Sabers, C.3
Wiederrecht, G.4
Lawrence J.C., Jr.5
Abraham, R.T.6
-
39
-
-
0030066934
-
Rapamycin blocks the phosphorylation of 4E-BP1 and inhibits cap-dependent initiation of translation
-
Beretta L, Gingras A-C, Svitkin YV, Hall MN, Sonenberg N. Rapamycin blocks the phosphorylation of 4E-BP1 and inhibits cap-dependent initiation of translation. EMBO J. 15:1996;658-664.
-
(1996)
EMBO J
, vol.15
, pp. 658-664
-
-
Beretta, L.1
Gingras A-C2
Svitkin, Y.V.3
Hall, M.N.4
Sonenberg, N.5
-
40
-
-
0030881836
-
Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin
-
of outstanding interest. This study demonstrates that a rapamycin-sensitive function of mTOR is required for insulin-stimulated PHAS-I phosphorylation in intact cells. Furthermore, mTOR is shown to phosphorylate PHAS-I directly in immune complex kinase assays. These results clarify the role of mTOR as a mitogen-stimulated effector of PHAS-I phosphorylation, and identify the first in vitro substrate for the mTOR kinase domain. These studies also suggest that rapamycin may inhibit cell growth by blocking the phosphorylation of PHAS-I by mTOR.
-
Brunn GJ, Hudson CC, Sekulic A, Williams JM, Hosoi H, Houghton PJ, Lawrence JC Jr, Abraham RT. Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin. of outstanding interest Science. 277:1997;99-101 This study demonstrates that a rapamycin-sensitive function of mTOR is required for insulin-stimulated PHAS-I phosphorylation in intact cells. Furthermore, mTOR is shown to phosphorylate PHAS-I directly in immune complex kinase assays. These results clarify the role of mTOR as a mitogen-stimulated effector of PHAS-I phosphorylation, and identify the first in vitro substrate for the mTOR kinase domain. These studies also suggest that rapamycin may inhibit cell growth by blocking the phosphorylation of PHAS-I by mTOR.
-
(1997)
Science
, vol.277
, pp. 99-101
-
-
Brunn, G.J.1
Hudson, C.C.2
Sekulic, A.3
Williams, J.M.4
Hosoi, H.5
Houghton, P.J.6
Lawrence J.C., Jr.7
Abraham, R.T.8
-
41
-
-
0031453135
-
The mammalian target of rapamycin phosphorylates sites having a (Ser/Thr)-Pro motif and is activated by antibodies to a region near its COOH terminus
-
of outstanding interest. The authors identify Thr36, Thr45, Ser64, Thr69 and Ser82 in PHAS-I as sites phosphorylated by mTOR in immune complex kinase assays. Interestingly, all five sites fit a (Ser/Thr)-Pro motif, supporting the idea that mTOR may be a proline-directed kinase. These findings are substantiated by Fadden et al., 1997 [42].
-
Brunn GJ, Fadden P, Haystead TAJ, Lawrence JC Jr. The mammalian target of rapamycin phosphorylates sites having a (Ser/Thr)-Pro motif and is activated by antibodies to a region near its COOH terminus. of outstanding interest J Biol Chem. 272:1997;32547-32550 The authors identify Thr36, Thr45, Ser64, Thr69 and Ser82 in PHAS-I as sites phosphorylated by mTOR in immune complex kinase assays. Interestingly, all five sites fit a (Ser/Thr)-Pro motif, supporting the idea that mTOR may be a proline-directed kinase. These findings are substantiated by Fadden et al., 1997 [42].
-
(1997)
J Biol Chem
, vol.272
, pp. 32547-32550
-
-
Brunn, G.J.1
Fadden, P.2
Haystead, T.A.J.3
Lawrence J.C., Jr.4
-
42
-
-
0030934285
-
Identification of phosphorylation sites in the translational regulator, PHAS-I, that are controlled by insulin and rapamycin in rat adipocytes
-
of special interest. In this report, the physiologic relevance of these phosphorylation events described by Brunn et al., 1997 [41] are substantiated by the finding that treatment of adipocytes with insulin provokes phosphorylation of the same five sites in PHAS-I. Rapamycin promotes the dephosphorylation of the sites at drug concentrations that interfere with the cellular response to insulin.
-
Fadden P, Haystead TAJ, Lawrence JC Jr. Identification of phosphorylation sites in the translational regulator, PHAS-I, that are controlled by insulin and rapamycin in rat adipocytes. of special interest J Biol Chem. 272:1997;10240-10247 In this report, the physiologic relevance of these phosphorylation events described by Brunn et al., 1997 [41] are substantiated by the finding that treatment of adipocytes with insulin provokes phosphorylation of the same five sites in PHAS-I. Rapamycin promotes the dephosphorylation of the sites at drug concentrations that interfere with the cellular response to insulin.
-
(1997)
J Biol Chem
, vol.272
, pp. 10240-10247
-
-
Fadden, P.1
Haystead, T.A.J.2
Lawrence J.C., Jr.3
-
43
-
-
0030013407
-
Both rapamycin-sensitive and -insensitive pathways are involved in the phosphorylation of the initiation factor-4E-binding protein (4E-BP1) in response to insulin in rat epididymal fat-cells
-
Diggle TA, Moule SK, Avison MB, Flynn A, Foulstone EJ, Proud CG, Denton RM. Both rapamycin-sensitive and -insensitive pathways are involved in the phosphorylation of the initiation factor-4E-binding protein (4E-BP1) in response to insulin in rat epididymal fat-cells. Biochem J. 316:1996;447-453.
-
(1996)
Biochem J
, vol.316
, pp. 447-453
-
-
Diggle, T.A.1
Moule, S.K.2
Avison, M.B.3
Flynn, A.4
Foulstone, E.J.5
Proud, C.G.6
Denton, R.M.7
-
44
-
-
0030013326
-
Stimulation of protein synthesis, eukaryotic translation initiation factor 4E phosphorylation, and PHAS-I phosphorylation by insulin requires insulin receptor substrate 1 and phosphatidylinositol 3-kinase
-
Mendez R, Myers MG Jr, White MF, Rhoads RE. Stimulation of protein synthesis, eukaryotic translation initiation factor 4E phosphorylation, and PHAS-I phosphorylation by insulin requires insulin receptor substrate 1 and phosphatidylinositol 3-kinase. Mol Cell Biol. 16:1996;2857-2864.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 2857-2864
-
-
Mendez, R.1
Myers M.G., Jr.2
White, M.F.3
Rhoads, R.E.4
-
45
-
-
0028963084
-
Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor
-
Yao R, Cooper GM. Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor. Science. 267:1995;2003-2006.
-
(1995)
Science
, vol.267
, pp. 2003-2006
-
-
Yao, R.1
Cooper, G.M.2
-
46
-
-
0028834557
-
Role of phosphatidylinositol 3-OH-kinase activity in the inhibition of apoptosis in haemopoietic cells: Phosphatidylinositol 3-OH-kinase inhibitors reveal a difference in signalling between interleukin-3 and granulocyte-macrophage colony stimulating factor
-
Scheid MP, Lauener RW, Duronio V. Role of phosphatidylinositol 3-OH-kinase activity in the inhibition of apoptosis in haemopoietic cells: phosphatidylinositol 3-OH-kinase inhibitors reveal a difference in signalling between interleukin-3 and granulocyte-macrophage colony stimulating factor. Biochem J. 312:1995;159-162.
-
(1995)
Biochem J
, vol.312
, pp. 159-162
-
-
Scheid, M.P.1
Lauener, R.W.2
Duronio, V.3
-
48
-
-
0030863160
-
Raf/MAPK and rapamycin-sensitive pathways mediate the anti-apoptotic function of p21Ras in IL-3-dependent hematopoietic cells
-
of special interest. This study demonstrates that oncogenic Ras prolongs the survival of an IL-3-dependent myeloid progenitor cell line cultured in the absence of cytokines. The authors use oncogenic Ras mutants containing single amino-acid substitutions in the effector domain to show that Ras is capable of delivering anti-apoptotic signals in the absence of MAP kinase activation. However, the cells are rendered significantly more sensitive to killing by rapamycin under these circumstances. The results of this study offer indirect evidence that mTOR is involved in the transmission of survival-promoting signals downstream of Ras in hematopoietic cells.
-
Kinoshita T, Shirouzu M, Kamiya A, Hashimoto K, Yokoyama S, Miyajima A. Raf/MAPK and rapamycin-sensitive pathways mediate the anti-apoptotic function of p21Ras in IL-3-dependent hematopoietic cells. of special interest Oncogene. 15:1997;619-627 This study demonstrates that oncogenic Ras prolongs the survival of an IL-3-dependent myeloid progenitor cell line cultured in the absence of cytokines. The authors use oncogenic Ras mutants containing single amino-acid substitutions in the effector domain to show that Ras is capable of delivering anti-apoptotic signals in the absence of MAP kinase activation. However, the cells are rendered significantly more sensitive to killing by rapamycin under these circumstances. The results of this study offer indirect evidence that mTOR is involved in the transmission of survival-promoting signals downstream of Ras in hematopoietic cells.
-
(1997)
Oncogene
, vol.15
, pp. 619-627
-
-
Kinoshita, T.1
Shirouzu, M.2
Kamiya, A.3
Hashimoto, K.4
Yokoyama, S.5
Miyajima, A.6
|