ArticleProceedings of the National Academy of Sciences of the United States of America1994
Spreading of differentiating human monocytes is associated with a major increase in membrane-bound CDC42.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 46 citations in OpenAlex.
- UPF1 regulates myeloid cell functions and S100A9 expression by the hnRNP E2/miRNA-328 balance.Scientific reports · 2016Article
- Staphylococcus aureus recruits Cdc42GAP through recycling endosomes and the exocyst to invade human endothelial cells.Journal of cell science · 2016Article
- Mixed lineage kinases (MLKs): a role in dendritic cells, inflammation and immunity?International journal of experimental pathology · 2007Review
- Actin can reorganize into podosomes in aortic endothelial cells, a process controlled by Cdc42 and RhoA.Molecular and cellular biology · 2003Article
- Regulation of Cdc42-mediated morphological effects: a novel function for p53.The EMBO journal · 2002Article
- RhoGDI-binding-defective mutant of Cdc42Hs targets to membranes and activates filopodia formation but does not cycle with the cytosol of mammalian cells.The Biochemical journal · 2001Article
- Coiling phagocytosis of Borrelia burgdorferi by primary human macrophages is controlled by CDC42Hs and Rac1 and involves recruitment of Wiskott-Aldrich syndrome protein and Arp2/3 complex.Infection and immunity · 2001Article
- Wiskott-Aldrich syndrome protein regulates podosomes in primary human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Cdc42: An essential Rho-type GTPase controlling eukaryotic cell polarity.Microbiology and molecular biology reviews : MMBR · 1999Review
- The Vav-Rac1 pathway in cytotoxic lymphocytes regulates the generation of cell-mediated killing.The Journal of experimental medicine · 1998Article
- RhoG GTPase controls a pathway that independently activates Rac1 and Cdc42Hs.Molecular biology of the cell · 1998Article
- ADP-ribosylation of the GTP-binding protein RhoA blocks cytoplasmic division in human myelomonocytic cells.The Biochemical journal · 1995Article
- Changes in tyrosine-phosphorylated p190 and its association with p120 type I and p100 type II rasGAPs during myelomonocytic differentiation of human leukemic cells.Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research · 1995Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In a search for a model cell system that might allow studies of the function of the Rho-related GTPase CDC42Hs in human cells, we measured the content and distribution of CDC42Hs in monocytes that were differentiating into macrophages. The total content of this protein increased 5- to 6-fold in phorbol ester-treated human monocytic THP-1 and U-937 cells and increased 13-fold in normal human blood monocytes. Moreover, membrane-associated CDC42Hs in these cells increased 13-fold and 30-fold, respectively, while cytosolic CDC42Hs increased only 3- and 6-fold. Measurements made specifically in U-937 cells showed that the increase in membrane CDC42Hs correlated closely with an increase in cell spreading. The changes in CDC42Hs in U-937 cells probably depended on increased mRNA translation and/or decreased protein degradation, since no change in CDC42Hs mRNA could be detected. Finally, the changes in CDC42Hs were relatively specific, since contents of the CDC42Hs-binding protein Rho-GDI and the Rho-related protein Rac2 were unaffected and no change in CDC42Hs occurred when the cells were stimulated by agonists that induce monocytes to differentiate into nonadherent cells. These findings show that marked changes in content and distribution of CDC42Hs occur when monocytes differentiate into macrophages, suggesting that membrane CDC42Hs may play a role in cell spreading.
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