Regulation of proliferation and apoptosis by Ras and Rho GTPases through specific phospholipid‐dependent signaling

FEBS Letters - Tập 410 Số 1 - Trang 73-77 - 1997
Juan Carlos Lacal1
1Instituto de Investigaciones Biomédicas, CSIC, Arturo Duperier 4, 28029 Madrid, Spain

Tóm tắt

Small GTPases are molecular switches that control signaling pathways critical for diverse cellular functions. Recent evidence indicates that multiple effector molecules can be activated by small GTPases. As a result, complex biological processes such as cell proliferation and apoptosis are turned on. Thus, rather than a single linear pathway from the membrane to the nucleus, the integration of complementary signals is required for these events to occur. In fact, the coordinated activation of small GTPases may constitute some of the critical modulators of those signals triggering either proliferation or cell death. In addition to the activation of specific kinases cascades, phospholipid‐derived messengers are candidates to compose some of the most critical elements associated to regulation of signaling cascades capable of discerning among life and death. Both proliferation and apoptosis needs competence and progression signals. Phospholipase D and sphingomyelinase may be important players in this decision‐maker step.

Từ khóa


Tài liệu tham khảo

Lacal J.C and McCormick F. (1993) The Ras superfamily of GTPases. CRC Press Boca Raton FL.

10.1002/bies.950170507

10.1016/S0968-0004(00)88991-4

10.1042/bj2880001

10.1096/fasebj.9.7.7737456

10.1038/358678a0

10.1038/358681a0

10.1016/0005-2760(94)90186-4

10.1038/330269a0

Cuadrado A., 1993, Oncogene, 8, 2959

10.1002/jcb.240570114

10.1002/nbm.1940050506

Bhakoo K.K., 1996, Cancer Res., 56, 4630

10.1038/323171a0

10.1016/S0021-9258(19)49864-5

10.1016/0304-4157(84)90010-8

10.1083/jcb.114.1.155

10.1083/jcb.121.6.1385

10.1016/S0021-9258(18)50065-X

Carnero A., 1994, Oncogene, 9, 1387

10.1128/MCB.9.1.325

10.1016/S0021-9258(19)39288-9

10.1006/abbi.1995.9959

10.1128/MCB.11.10.4903

10.1042/bj3220519

Lacal J.C., 1994, Oncol. Rep., 1, 677

10.1128/MCB.15.2.1094

10.1002/jcb.240520408

Esteve P., 1995, Oncogene, 11, 2657

10.1016/0092-8674(93)90323-I

10.1126/science.8290961

10.1038/378409a0

10.1016/S0021-9258(18)82288-8

10.1016/S0968-0004(00)88961-6

10.1038/378307a0

10.1038/380075a0

10.1038/381800a0

10.1074/jbc.272.5.3064

Perona R., 1993, Oncogene, 8, 1285

10.1128/MCB.15.11.6443

10.1038/374457a0

10.1038/385544a0

Rodriguez-Viciana P. Warne P.H. Khwaja A. Marte B.M. Pappin D.J. Das P. Waterfield M.D. Ridley A. and Downward J. (1997) Cell in press.

Khwaja A. Rodrı́guez-Viciana P. Wennstrom S. Wane P.H. and Downward J. (1997) EMBO J. in press.

Jiménez B., 1995, Oncogene, 10, 811

10.1016/S0021-9258(19)74497-4

10.1016/0092-8674(94)90259-3

10.1126/science.271.5249.648

10.1002/j.1460-2075.1996.tb00539.x

10.1038/367040a0

10.1002/j.1460-2075.1996.tb00574.x

10.1002/j.1460-2075.1995.tb00281.x

10.1126/science.271.5249.645

10.1126/science.273.5272.245

10.1016/S0092-8674(05)80019-4

10.1016/S0092-8674(05)80018-2

10.1016/S0092-8674(05)80020-0

10.1101/gad.11.4.463

10.1038/nm0197-20