This item requires a subscription to Journal of Leukocyte Biology.
Full Text (PDF)
Statins inhibit T-ALL cell chemotaxis, transendothelial migration, and adhesion to ICAM-1, which correlates with reduced function of the GTPase Rap1b but not Rap1a.
To view this item, select one of the options below:
Sign In
Join the Society for Leukocyte Biology and Receive an Online Subscription as a Member Benefit
If you find yourself repeatedly purchasing articles in the journal, society membership may be more cost-effective. Click here to apply online. Please note that joining the society may take several days or weeks as your application is reviewed. As a result, you WILL
NOT have immediate access to this article by applying online.
Purchase Short-Term Access
- Pay per Article - You may access and print this article (from the computer you are currently using) for 1 day for US$20.00.
- Regain Access - You can regain access to a recent Pay per Article purchase and print it if your access period has not yet expired.
Subscribe to the Journal
- Subscribe to the Journal - Subscribe to the print and/or online journal.
This Article
-
April 2011 Journal of Leukocyte Biology vol. 89 no. 4 577-586
- Show PDF in full window
- AbstractFree
- Full Text
- » Full Text (PDF)
- PDF + Supp Data
- Supplemental Figures and Movies
-
All Versions of this Article:
- jlb.0810441v1
- 89/4/577 most recent
- Buy
Article Usage Stats
Classifications
Services
Citing Articles
Google Scholar
PubMed
Related Content
Current Issue
From the Cover
- Editorial: IL-2/IL-2R axis modulation by mesenchymal stromal cells: interaction with immunosuppressive drugs?
- Editorial: Binge drinking: lessons from ATF3 and HDAC1 collaboration.
- Frontline Science: Placenta-derived decidual stromal cells alter IL-2R expression and signaling in alloantigen-activated T cells.
- Frontline Science: ATF3 is responsible for the inhibition of TNF-α release and the impaired migration of acute ethanol-exposed monocytes and macrophages.
- Technical Advance: Changes in neutrophil migration patterns upon contact with platelets in a microfluidic assay.
