Journal
EXPERIMENTAL CELL RESEARCH
Volume 310, Issue 2, Pages 303-310Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2005.07.015
Keywords
-
Categories
Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000M050] Funding Source: researchfish
- Medical Research Council [G117/424] Funding Source: researchfish
- MRC [G117/424] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000M050] Funding Source: Medline
- Medical Research Council [G117/424] Funding Source: Medline
Ask authors/readers for more resources
Vav family proteins act as guanine nucleotide exchange factors for Rho family proteins, which are known to orchestrate cytoskeletal changes and cell migration in response to extracellular stimuli. Using mice deficient for Vav1, Vav2 and/or Vav3, overlapping and isoform-specific functions of the three Vav proteins have been described in various hematopoietic cell types, but their roles in regulating cell morphology and migration have not been studied in detail. To investigate whether Vav isoforms have redundant or unique functions in regulating adhesion and migration, we investigated the properties of Vav1-deficient and Vav2-deficient macrophages. Both Vav1-deficient and Vav2-deficient cells have a smaller adhesive area; yet, only Vav1-deficient cells have a reduced migration speed, which coincides with a lower level of microtubules. Vav2-deficient inacrophages display a high level of constitutive membrane ruffling, but neither Vav1 nor Vav2 is required for colony stimulating factor-1-induced membrane ruffling and cell spreading. Our results suggest that the migration speed of macrophages is regulated independently of spread area or membrane ruffling and that Vav1 is selectively required to maintain a normal migration speed. (c) 2005 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available