{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:16:13Z","timestamp":1791418573036,"version":"4.3.3"},"reference-count":34,"publisher":"Rockefeller University Press","issue":"4","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,8,20]]},"abstract":"<jats:p>Capping the barbed ends of actin filaments is a critical step for regulating actin-based motility in nonmuscle cells. The in vivo function of CapG, a calcium-sensitive barbed end capping protein and member of the gelsolin\/villin family, has been assessed using a null Capg allele engineered into mice. Both CapG-null mice and CapG\/gelsolin double-null mice appear normal and have no gross functional abnormalities. However, the loss of CapG in bone marrow macrophages profoundly inhibits macrophage colony stimulating factor\u2013stimulated ruffling; reintroduction of CapG protein by microinjection fully restores this function. CapG-null macrophages also demonstrate \u223c50% impairment of immunoglobulin G, and complement-opsonized phagocytosis and lanthanum-induced vesicle rocketing. These motile functions are not impaired in gelsolin-null macrophages and no additive effects are observed in CapG\/gelsolin double-null macrophages, establishing that CapG function is distinct from, and does not overlap with, gelsolin in macrophages. Our observations indicate that CapG is required for receptor-mediated ruffling, and that it is a major functional component of macrophage phagocytosis. These primary effects on macrophage motile function suggest that CapG may be a useful target for the regulation of macrophage-mediated inflammatory responses.<\/jats:p>","DOI":"10.1083\/jcb.200101113","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T12:46:23Z","timestamp":1027687583000},"page":"775-784","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":138,"title":["Comparisons of CapG and gelsolin-null macrophages"],"prefix":"10.1083","volume":"154","author":[{"given":"Walter","family":"Witke","sequence":"first","affiliation":[{"name":"1Hematology Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"2Infectious Disease Division, Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J.","family":"Kwiatkowski","sequence":"additional","affiliation":[{"name":"1Hematology Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick S.","family":"Southwick","sequence":"additional","affiliation":[{"name":"2Infectious Disease Division, Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2001,8,20]]},"reference":[{"key":"2023072904315459700_BIB1","doi-asserted-by":"crossref","first-page":"601","DOI":"10.1084\/jem.179.2.601","volume":"179","year":"1994","journal-title":"J. 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