Two GTPases, Cdc42 and Rac, bind directly to a protein implicated in the immunodeficiency disorder Wiskott–Aldrich syndrome
- 1 January 1996
- journal article
- Published by Elsevier in Current Biology
- Vol. 6 (1) , 70-75
- https://doi.org/10.1016/s0960-9822(02)00423-2
Abstract
No abstract availableKeywords
This publication has 36 references indexed in Scilit:
- Selective activation of the JNK signaling cascadeand c-Jun transcriptional activity by the small GTPases Rac and Cdc42HsCell, 1995
- The small GTP-binding proteins Rac1 and Cdc42regulate the activity of the JNK/SAPK signaling pathwayCell, 1995
- Getting the actin filaments straight: nucleation-release or treadmilling?Trends in Cell Biology, 1995
- Small GTP-Binding Proteins and the Regulation of the Actin CytoskeletonAnnual Review of Cell Biology, 1994
- Direct interaction of Ras and the amino-terminal region of Raf-1 in vitroNature, 1993
- Normal and oncogenic p21ras proteins bind to the amino-terminal regulatory domain of c-Raf-1Nature, 1993
- Evidence for defective transmembrane signaling in B cells from patients with Wiskott-Aldrich syndrome.Journal of Clinical Investigation, 1992
- The small GTP-binding protein rac regulates growth factor-induced membrane rufflingCell, 1992
- The small GTP-binding protein rho regulates the assembly of focal adhesions and actin stress fibers in response to growth factorsCell, 1992
- Polarity of actin at the leading edge of cultured cellsNature, 1978