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Cited by 572

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Rac and Cdc42 Induce Actin Polymerization and G1 Cell Cycle Progression Independently of p65PAK and the JNK/SAPK MAP Kinase Cascade

Open access
Lamarche, Nathalie, Tapon, Nicolas, Stowers, Lisa, Burbelo, Peter D, Aspenström, Pontus, Bridges, Tina, Chant, John, Hall, Alan·1996·Cell

Abstract

Rac and Cdc42 regulate a variety of responses in mammalian cells including formation of lamellipodia and filopodia, activation of the JNK MAP kinase cascade, and induction of G1 cell cycle progression. Rac is also one of the downstream targets required for Ras-induced malignant transformation. Rac and Cdc42 containing a Y40C effector site substitution no longer intact with the Ser/Thr kinase p65PAK and are unable to activate the JNK MAP kinase pathway. However, they still induce cytoskeletal changes and G1 cell cycle progression. Rac containing an F37A effector site substitution, on the other hand, no longer interacts with the Ser/Thr kinase p160ROCK and is unable to induce lamellipodia or G1 progression. We conclude that Rac and Cdc42 control MAP kinase pathways and actin cytoskeleton organization independently through distinct downstream targets.

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Metadata

Authors
Lamarche, N., Tapon, N., Stowers, L., Burbelo, P. D., Aspenström, P., Bridges, T., Chant, J., & Hall, A.
Venue
Cell
Publisher
Elsevier BV
Published
1996-11
Volume
87
Issue
3
Pages
519-529
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2002410732
Cited by
572
References
0
FWCI
22.88
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Rac and Cdc42 Induce Actin Polymerization and G1 Cell Cycle Progression Independently of p65PAK and the JNK/SAPK MAP Kinase Cascade. https://app.cochat.ai/papers/10.1016/s0092-8674(00)81371-9
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Lamarche, N., Tapon, N., Stowers, L., Burbelo, P. D., Aspenström, P., Bridges, T., Chant, J., & Hall, A. (1996). Rac and Cdc42 Induce Actin Polymerization and G1 Cell Cycle Progression Independently of p65PAK and the JNK/SAPK MAP Kinase Cascade. Cell. https://doi.org/10.1016/s0092-8674(00)81371-9

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