{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:01:45Z","timestamp":1791223305264,"version":"4.1.0"},"reference-count":50,"publisher":"The Company of Biologists","issue":"22","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,11,15]]},"abstract":"<jats:p>Colony-stimulating factor 1 (CSF-1) is an important physiological chemoattractant for macrophages. The mechanisms by which CSF-1 elicits the formation of filamentous actin (F-actin)-rich membrane protrusions and induces macrophage migration are not fully understood. In particular, very little is known regarding the contribution of the different members of the Wiskott-Aldrich Syndrome protein (WASP) family of actin regulators in response to CSF-1. Although a role for WASP itself in macrophage chemotaxis has been previously identified, no data was available regarding the function of WASP family verprolin-homologous (WAVE) proteins in this cell type. We found that WAVE2 was the predominant isoform to be expressed in primary macrophages and in cells derived from the murine monocyte\/macrophage RAW264.7 cell line (RAW\/LR5). CSF-1 treatment of macrophages resulted in WAVE2 accumulation in F-actin-rich protrusions induced by CSF-1. Inhibition of WAVE2 function by expressing a dominant-negative mutant or introducing anti-WAVE2 antibodies in RAW\/LR5 cells, as well as reduction of endogenous WAVE2 expression by RNA-mediated interference (RNAi), resulted in a significant reduction of CSF-1-elicited F-actin protrusions. WAVE2 was found in a protein complex together with Abelson kinase interactor 1 (Abi1) in resting or stimulated cells. Both WAVE2 and Abi1 were recruited to and necessary for the formation of F-actin protrusions in response to CSF-1. Reducing the levels of WAVE2, directly or by targeting Abi1, resulted in an impaired cell migration to CSF-1. Altogether these data identify a WAVE2-Abi1 complex crucial for the normal actin cytoskeleton reorganization and migration of macrophages in response to CSF-1.<\/jats:p>","DOI":"10.1242\/jcs.02638","type":"journal-article","created":{"date-parts":[[2005,11,9]],"date-time":"2005-11-09T21:33:38Z","timestamp":1131572018000},"page":"5369-5379","source":"Crossref","is-referenced-by-count":75,"title":["A WAVE2-Abi1 complex mediates CSF-1-induced F-actin-rich membrane protrusions and migration in macrophages"],"prefix":"10.1242","volume":"118","author":[{"given":"Wassim","family":"Abou Kheir","sequence":"first","affiliation":[{"name":"Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Claude","family":"Gevrey","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideki","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beth","family":"Isaac","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dianne","family":"Cox","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"},{"name":"Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York City, NY 10461, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042519094546000_REF1","doi-asserted-by":"crossref","unstructured":"Abell, A. 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