|
|
Blood, 15 April 2005, Vol. 105, No. 8, pp. 3026-3034.
Prepublished online as a Blood First Edition Paper on December 23, 2004; DOI 10.1182/blood-2004-07-2925.
 Previous Article | Table of Contents | Next Article 
CHEMOKINES
Control of lymphocyte shape and the chemotactic response by the GTP exchange factor Vav
Miguel Vicente-Manzanares,
Aranzazu Cruz-Adalia,
Noa B. Martín-Cófreces,
José R. Cabrero,
Mercedes Dosil,
Brenda Alvarado-Sánchez,
Xosé R. Bustelo, and
Francisco Sánchez-Madrid
From the Servicio de Inmunología, Hospital Universitario de la Princesa, Madrid, Spain; Centro de Investigación del Cáncer (CIC), Campus Miguel de Unamuno, Salamanca, Spain; and Facultad de Medicina, Universidad Autónoma de San Luis Potosí (UASLP), San Luis Potosí, Mexico.
Rho GTPases control many facets of cell polarity and migration; namely, the reorganization of the cellular cytoskeleton to extracellular stimuli. Rho GTPases are activated by GTP exchange factors (GEFs), which induce guanosine diphosphate (GDP) release and the stabilization of the nucleotide-free state. Thus, the role of GEFs in the regulation of the cellular response to extracellular cues during cell migration is a critical step of this process. In this report, we have analyzed the activation and subcellular localization of the hematopoietic GEF Vav in human peripheral blood lymphocytes stimulated with the chemokine stromal cell–derived factor-1 (SDF-1 ). We show a robust activation of Vav and its redistribution to motility-associated subcellular structures, and we provide biochemical evidence of the recruitment of Vav to the membrane of SDF-1–activated human lymphocytes, where it transiently interacts with the SDF-1 receptor CXCR4. Overexpression of a dominant negative form of Vav abolished lymphocyte polarization, actin polymerization, and migration. SDF-1–mediated cell polarization and migration also were impaired by overexpression of an active, oncogenic Vav, although the mechanism appears to be different. Together, our data postulate a pivotal role for Vav in the transmission of the migratory signal through the chemokine receptor CXCR4.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
M. M. Escribese, E. Conde, D. Saenz-Morales, P. L. Hordijk, and M. L. Garcia-Bermejo
Mononuclear Cell Extravasation in an Inflammatory Response Is Abrogated by All-Trans-Retinoic Acid through Inhibiting the Acquisition of an Appropriate Migratory Phenotype
J. Pharmacol. Exp. Ther.,
February 1, 2008;
324(2):
454 - 462.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Patrussi, C. Ulivieri, O. M. Lucherini, S. R. Paccani, A. Gamberucci, L. Lanfrancone, P. G. Pelicci, and C. T. Baldari
p52Shc is required for CXCR4-dependent signaling and chemotaxis in T cells
Blood,
September 15, 2007;
110(6):
1730 - 1738.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Wei, S. da Rocha Dias, H. Wang, and C. E. Rudd
CTL-Associated Antigen-4 Ligation Induces Rapid T Cell Polarization That Depends on Phosphatidylinositol 3-Kinase, Vav-1, Cdc42, and Myosin Light Chain Kinase
J. Immunol.,
July 1, 2007;
179(1):
400 - 408.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Jolly, I. Mitar, and Q. J. Sattentau
Requirement for an Intact T-Cell Actin and Tubulin Cytoskeleton for Efficient Assembly and Spread of Human Immunodeficiency Virus Type 1
J. Virol.,
June 1, 2007;
81(11):
5547 - 5560.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Gerard, A. E.E. Mertens, R. A. van der Kammen, and J. G. Collard
The Par polarity complex regulates Rap1- and chemokine-induced T cell polarization
J. Cell Biol.,
March 12, 2007;
176(6):
863 - 875.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. Tan, D. Martin, and J. S. Gutkind
The G{alpha}13-Rho Signaling Axis Is Required for SDF-1-induced Migration through CXCR4
J. Biol. Chem.,
December 22, 2006;
281(51):
39542 - 39549.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Schymeinsky, A. Sindrilaru, D. Frommhold, M. Sperandio, R. Gerstl, C. Then, A. Mocsai, K. Scharffetter-Kochanek, and B. Walzog
The Vav binding site of the non-receptor tyrosine kinase Syk at Tyr 348 is critical for beta2 integrin (CD11/CD18)-mediated neutrophil migration
Blood,
December 1, 2006;
108(12):
3919 - 3927.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Schapira, G. Lazer, and S. Katzav
Osteopontin Is an Oncogenic Vav1- but not Wild-type Vav1-Responsive Gene: Implications for Fibroblast Transformation.
Cancer Res.,
June 15, 2006;
66(12):
6183 - 6191.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
