Activation of Rac-1, Rac-2, and Cdc42 by hemopoietic growth factors or cross-linking of the B-lymphocyte receptor for antigen
Interleukin-3 (IL-3)–induced activation of endogenous Rac-1, Rac-2, and Cdc42. Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 or by cross-linking the B-lymphocyte receptor for antigen (BCR...
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description | Interleukin-3 (IL-3)–induced activation of endogenous Rac-1, Rac-2, and Cdc42. Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 or by cross-linking the B-lymphocyte receptor for antigen (BCR). The activation of Rac-1 induced by cross-linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with about 25% to 30% of Rac-1 activation still occurring in the absence of detectable increases in phosphatidyl-inositol-3 kinase (PI-3K) activity. Overexpression of constitutively active mutants of H-Ras, N-Ras, or M-Ras resulted in activation of coexpressed Rac-1 through an Ly29402-resistant, PI-3K–independent mechanism. Overexpression of constitutively active mutants of p21 Ras, or Rac-1, but not of PI-3K, was sufficient for activation of p38 mitogen-activated protein kinase (MAPK) in cells of hemopoietic origin. Inhibition of increases in PI-3K activity by Ly294002 had no effect on the IL-3–induced activation of p38 MAPK. In contrast, Ly294002 partially inhibited the activation of p38 MAPK induced by cross-linking of the BCR, although some p38 MAPK activation occurred in the absence of increases in the activity of Rac-1 or PI-3K. The activation of Rac-1, Rac-2, and Cdc42 by IL-3 and other hemopoietic growth factors is likely to be an important component of their actions in promoting growth, survival, and function. |
doi_str_mv | 10.1182/blood-2002-01-0154 |
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Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 or by cross-linking the B-lymphocyte receptor for antigen (BCR). The activation of Rac-1 induced by cross-linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with about 25% to 30% of Rac-1 activation still occurring in the absence of detectable increases in phosphatidyl-inositol-3 kinase (PI-3K) activity. Overexpression of constitutively active mutants of H-Ras, N-Ras, or M-Ras resulted in activation of coexpressed Rac-1 through an Ly29402-resistant, PI-3K–independent mechanism. Overexpression of constitutively active mutants of p21 Ras, or Rac-1, but not of PI-3K, was sufficient for activation of p38 mitogen-activated protein kinase (MAPK) in cells of hemopoietic origin. Inhibition of increases in PI-3K activity by Ly294002 had no effect on the IL-3–induced activation of p38 MAPK. In contrast, Ly294002 partially inhibited the activation of p38 MAPK induced by cross-linking of the BCR, although some p38 MAPK activation occurred in the absence of increases in the activity of Rac-1 or PI-3K. The activation of Rac-1, Rac-2, and Cdc42 by IL-3 and other hemopoietic growth factors is likely to be an important component of their actions in promoting growth, survival, and function.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2002-01-0154</identifier><identifier>PMID: 12384416</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Bone Marrow Cells - drug effects ; Bone Marrow Cells - metabolism ; cdc42 GTP-Binding Protein - drug effects ; cdc42 GTP-Binding Protein - metabolism ; Cell differentiation, maturation, development, hematopoiesis ; Cell Line - drug effects ; Cell Line - metabolism ; Cell physiology ; Chromones - pharmacology ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Genes, ras ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Hematopoietic Cell Growth Factors - pharmacology ; Hematopoietic Stem Cells - drug effects ; Hematopoietic Stem Cells - metabolism ; Interleukin-3 - pharmacology ; Interleukin-5 - pharmacology ; Macrophage Colony-Stimulating Factor - pharmacology ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - metabolism ; Molecular and cellular biology ; Morpholines - pharmacology ; p38 Mitogen-Activated Protein Kinases ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - pharmacology ; Phosphoinositide-3 Kinase Inhibitors ; Proto-Oncogene Proteins p21(ras) - physiology ; rac GTP-Binding Proteins - drug effects ; rac GTP-Binding Proteins - metabolism ; rac1 GTP-Binding Protein - drug effects ; rac1 GTP-Binding Protein - genetics ; rac1 GTP-Binding Protein - metabolism ; RAC2 GTP-Binding Protein ; Receptors, Antigen, B-Cell - immunology ; Stem Cell Factor - pharmacology</subject><ispartof>Blood, 2002-11, Vol.100 (9), p.3183-3192</ispartof><rights>2002 American Society of Hematology</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-b96ff4ee1685fefcca4a2fc69a6fc855f7f414cc0bdc8a008ed3975e1b0b40c63</citedby><cites>FETCH-LOGICAL-c448t-b96ff4ee1685fefcca4a2fc69a6fc855f7f414cc0bdc8a008ed3975e1b0b40c63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14525204$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12384416$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grill, Brock</creatorcontrib><creatorcontrib>Schrader, John W.</creatorcontrib><title>Activation of Rac-1, Rac-2, and Cdc42 by hemopoietic growth factors or cross-linking of the B-lymphocyte receptor for antigen</title><title>Blood</title><addtitle>Blood</addtitle><description>Interleukin-3 (IL-3)–induced activation of endogenous Rac-1, Rac-2, and Cdc42. Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 or by cross-linking the B-lymphocyte receptor for antigen (BCR). The activation of Rac-1 induced by cross-linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with about 25% to 30% of Rac-1 activation still occurring in the absence of detectable increases in phosphatidyl-inositol-3 kinase (PI-3K) activity. Overexpression of constitutively active mutants of H-Ras, N-Ras, or M-Ras resulted in activation of coexpressed Rac-1 through an Ly29402-resistant, PI-3K–independent mechanism. Overexpression of constitutively active mutants of p21 Ras, or Rac-1, but not of PI-3K, was sufficient for activation of p38 mitogen-activated protein kinase (MAPK) in cells of hemopoietic origin. Inhibition of increases in PI-3K activity by Ly294002 had no effect on the IL-3–induced activation of p38 MAPK. In contrast, Ly294002 partially inhibited the activation of p38 MAPK induced by cross-linking of the BCR, although some p38 MAPK activation occurred in the absence of increases in the activity of Rac-1 or PI-3K. The activation of Rac-1, Rac-2, and Cdc42 by IL-3 and other hemopoietic growth factors is likely to be an important component of their actions in promoting growth, survival, and function.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Cells - drug effects</subject><subject>Bone Marrow Cells - metabolism</subject><subject>cdc42 GTP-Binding Protein - drug effects</subject><subject>cdc42 GTP-Binding Protein - metabolism</subject><subject>Cell differentiation, maturation, development, hematopoiesis</subject><subject>Cell Line - drug effects</subject><subject>Cell Line - metabolism</subject><subject>Cell physiology</subject><subject>Chromones - pharmacology</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genes, ras</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Hematopoietic Cell Growth Factors - pharmacology</subject><subject>Hematopoietic Stem Cells - drug effects</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Interleukin-3 - pharmacology</subject><subject>Interleukin-5 - pharmacology</subject><subject>Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>MAP Kinase Signaling System</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Molecular and cellular biology</subject><subject>Morpholines - pharmacology</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - pharmacology</subject><subject>Phosphoinositide-3 Kinase Inhibitors</subject><subject>Proto-Oncogene Proteins p21(ras) - physiology</subject><subject>rac GTP-Binding Proteins - drug effects</subject><subject>rac GTP-Binding Proteins - metabolism</subject><subject>rac1 GTP-Binding Protein - drug effects</subject><subject>rac1 GTP-Binding Protein - genetics</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>RAC2 GTP-Binding Protein</subject><subject>Receptors, Antigen, B-Cell - immunology</subject><subject>Stem Cell Factor - pharmacology</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMGKFDEQhoMo7uzqC3iQXPS00SST7k6Dl93BVWFBED2HdHVlJtrdaZPMyhx8d9MzA3sTqigIX_1UPkJeCf5OCC3fd0MIPZOcS8ZFqUo9IStRSc3KE39KVpzzmqm2ERfkMqWfnAu1ltVzciHkWisl6hX5ewPZP9jsw0SDo98sMHF9HPKa2qmnmx6UpN2B7nAMc_CYPdBtDH_yjjoLOcREQ6QQQ0ps8NMvP22XpLxDesuGwzjvAhwy0oiAc8GpK22n7Lc4vSDPnB0SvjzPK_Lj7uP3zWd2__XTl83NPQOldGZdWzunEEWtK4cOwCorHdStrR3oqnKNU0IB8K4HbTnX2K_bpkLR8U5xqNdX5O0pd47h9x5TNqNPgMNgJwz7ZBopGi10W0B5Ao__iejMHP1o48EIbhbp5ijdLNINF2aRXpZen9P33Yj948rZcgHenAGbwA4u2gl8euRUJSvJl6APJw6LiweP0STwOAH2vtjLpg_-f3f8A-_6oGw</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>Grill, Brock</creator><creator>Schrader, John W.</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20021101</creationdate><title>Activation of Rac-1, Rac-2, and Cdc42 by hemopoietic growth factors or cross-linking of the B-lymphocyte receptor for antigen</title><author>Grill, Brock ; Schrader, John W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-b96ff4ee1685fefcca4a2fc69a6fc855f7f414cc0bdc8a008ed3975e1b0b40c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Bone Marrow Cells - metabolism</topic><topic>cdc42 GTP-Binding Protein - drug effects</topic><topic>cdc42 GTP-Binding Protein - metabolism</topic><topic>Cell differentiation, maturation, development, hematopoiesis</topic><topic>Cell Line - drug effects</topic><topic>Cell Line - metabolism</topic><topic>Cell physiology</topic><topic>Chromones - pharmacology</topic><topic>Enzyme Activation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genes, ras</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Hematopoietic Cell Growth Factors - pharmacology</topic><topic>Hematopoietic Stem Cells - drug effects</topic><topic>Hematopoietic Stem Cells - metabolism</topic><topic>Interleukin-3 - pharmacology</topic><topic>Interleukin-5 - pharmacology</topic><topic>Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>MAP Kinase Signaling System</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Molecular and cellular biology</topic><topic>Morpholines - pharmacology</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - pharmacology</topic><topic>Phosphoinositide-3 Kinase Inhibitors</topic><topic>Proto-Oncogene Proteins p21(ras) - physiology</topic><topic>rac GTP-Binding Proteins - drug effects</topic><topic>rac GTP-Binding Proteins - metabolism</topic><topic>rac1 GTP-Binding Protein - drug effects</topic><topic>rac1 GTP-Binding Protein - genetics</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>RAC2 GTP-Binding Protein</topic><topic>Receptors, Antigen, B-Cell - immunology</topic><topic>Stem Cell Factor - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grill, Brock</creatorcontrib><creatorcontrib>Schrader, John W.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grill, Brock</au><au>Schrader, John W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Rac-1, Rac-2, and Cdc42 by hemopoietic growth factors or cross-linking of the B-lymphocyte receptor for antigen</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>100</volume><issue>9</issue><spage>3183</spage><epage>3192</epage><pages>3183-3192</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Interleukin-3 (IL-3)–induced activation of endogenous Rac-1, Rac-2, and Cdc42. Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 or by cross-linking the B-lymphocyte receptor for antigen (BCR). The activation of Rac-1 induced by cross-linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with about 25% to 30% of Rac-1 activation still occurring in the absence of detectable increases in phosphatidyl-inositol-3 kinase (PI-3K) activity. Overexpression of constitutively active mutants of H-Ras, N-Ras, or M-Ras resulted in activation of coexpressed Rac-1 through an Ly29402-resistant, PI-3K–independent mechanism. Overexpression of constitutively active mutants of p21 Ras, or Rac-1, but not of PI-3K, was sufficient for activation of p38 mitogen-activated protein kinase (MAPK) in cells of hemopoietic origin. Inhibition of increases in PI-3K activity by Ly294002 had no effect on the IL-3–induced activation of p38 MAPK. In contrast, Ly294002 partially inhibited the activation of p38 MAPK induced by cross-linking of the BCR, although some p38 MAPK activation occurred in the absence of increases in the activity of Rac-1 or PI-3K. The activation of Rac-1, Rac-2, and Cdc42 by IL-3 and other hemopoietic growth factors is likely to be an important component of their actions in promoting growth, survival, and function.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>12384416</pmid><doi>10.1182/blood-2002-01-0154</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Bone Marrow Cells - drug effects Bone Marrow Cells - metabolism cdc42 GTP-Binding Protein - drug effects cdc42 GTP-Binding Protein - metabolism Cell differentiation, maturation, development, hematopoiesis Cell Line - drug effects Cell Line - metabolism Cell physiology Chromones - pharmacology Enzyme Activation Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Genes, ras Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Hematopoietic Cell Growth Factors - pharmacology Hematopoietic Stem Cells - drug effects Hematopoietic Stem Cells - metabolism Interleukin-3 - pharmacology Interleukin-5 - pharmacology Macrophage Colony-Stimulating Factor - pharmacology MAP Kinase Signaling System Mice Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism Molecular and cellular biology Morpholines - pharmacology p38 Mitogen-Activated Protein Kinases Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - pharmacology Phosphoinositide-3 Kinase Inhibitors Proto-Oncogene Proteins p21(ras) - physiology rac GTP-Binding Proteins - drug effects rac GTP-Binding Proteins - metabolism rac1 GTP-Binding Protein - drug effects rac1 GTP-Binding Protein - genetics rac1 GTP-Binding Protein - metabolism RAC2 GTP-Binding Protein Receptors, Antigen, B-Cell - immunology Stem Cell Factor - pharmacology |
title | Activation of Rac-1, Rac-2, and Cdc42 by hemopoietic growth factors or cross-linking of the B-lymphocyte receptor for antigen |
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