c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion
Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show th...
Gespeichert in:
| Veröffentlicht in: | The Journal of immunology (1950) 2009-03, Vol.182 (5), p.3233-3242 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 3242 |
|---|---|
| container_issue | 5 |
| container_start_page | 3233 |
| container_title | The Journal of immunology (1950) |
| container_volume | 182 |
| creator | Cui, Lingling Chen, Cuixia Xu, Ting Zhang, Juechao Shang, Xin Luo, Jixian Chen, Liang Ba, Xueqing Zeng, Xianlu |
| description | Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show that c-Abl kinase is activated by beta(2) integrin engagement and is required for beta(2) integrin-dependent neutrophil sustained adhesion and spreading. The expression of beta(2) integrin on neutrophils induced by TNF-alpha is not affected by c-Abl kinase inhibitor STI571, suggesting that c-Abl kinase is not involved in TNF-alpha-induced integrin activation. The recruitment of c-Abl kinase to beta(2) integrin is dependent on talin head domain, which constitutively interacts with beta(2) integrin cytoplasmic domain. After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav. The SH3 domain of c-Abl kinase is involved in its interaction with talin and Vav. Thus, c-Abl kinase plays an essential role in the activation of Vav induced by beta(2) integrin ligation and in regulating neutrophil-sustained adhesion and spreading. |
| doi_str_mv | 10.4049/jimmunol.0802621 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_66952747</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>66952747</sourcerecordid><originalsourceid>FETCH-LOGICAL-p541-522183f79a1142d028994a325652f63d63e682762485315471712d52963b87f3</originalsourceid><addsrcrecordid>eNo1jztPwzAUhS0kREthZ0Ke2FLsa_s6HquKR6VKDLBHTuNQl8RJ7Xjg3xMJmM5wPp0HIXecrSWT5vHk-z6HoVuzkgECvyBLrhQrEBkuyHVKJ8YYMpBXZMENCAnAl2R3KDZ1R798sMlRn2h05-yja2g7RFq7yVKgPkzuM_pQ9K7xdprN4PIUh_HoO2qbo0t-CDfksrVdcrd_uiLvz08f29di__ay2272xagkL9TcWopWG8u5hIZBaYy0AhQqaFE0KByWoBFkqQRXUnPNoVFgUNSlbsWKPPymjnE4Z5emqvfp4LrOBjfkVCEaBVrqGbz_A3M9z67G6Hsbv6v_6-IHfbFXxw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>66952747</pqid></control><display><type>article</type><title>c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Cui, Lingling ; Chen, Cuixia ; Xu, Ting ; Zhang, Juechao ; Shang, Xin ; Luo, Jixian ; Chen, Liang ; Ba, Xueqing ; Zeng, Xianlu</creator><creatorcontrib>Cui, Lingling ; Chen, Cuixia ; Xu, Ting ; Zhang, Juechao ; Shang, Xin ; Luo, Jixian ; Chen, Liang ; Ba, Xueqing ; Zeng, Xianlu</creatorcontrib><description>Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show that c-Abl kinase is activated by beta(2) integrin engagement and is required for beta(2) integrin-dependent neutrophil sustained adhesion and spreading. The expression of beta(2) integrin on neutrophils induced by TNF-alpha is not affected by c-Abl kinase inhibitor STI571, suggesting that c-Abl kinase is not involved in TNF-alpha-induced integrin activation. The recruitment of c-Abl kinase to beta(2) integrin is dependent on talin head domain, which constitutively interacts with beta(2) integrin cytoplasmic domain. After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav. The SH3 domain of c-Abl kinase is involved in its interaction with talin and Vav. Thus, c-Abl kinase plays an essential role in the activation of Vav induced by beta(2) integrin ligation and in regulating neutrophil-sustained adhesion and spreading.</description><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.0802621</identifier><identifier>PMID: 19234221</identifier><language>eng</language><publisher>United States</publisher><subject>CD18 Antigens - metabolism ; CD18 Antigens - physiology ; Cell Adhesion - immunology ; Cytoplasm - enzymology ; Cytoplasm - immunology ; Cytoplasm - metabolism ; HL-60 Cells ; Humans ; Neutrophil Activation - immunology ; Neutrophils - cytology ; Neutrophils - enzymology ; Neutrophils - immunology ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-abl - metabolism ; Proto-Oncogene Proteins c-abl - physiology ; Signal Transduction - immunology ; Talin - physiology ; Tumor Necrosis Factor-alpha - physiology</subject><ispartof>The Journal of immunology (1950), 2009-03, Vol.182 (5), p.3233-3242</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19234221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cui, Lingling</creatorcontrib><creatorcontrib>Chen, Cuixia</creatorcontrib><creatorcontrib>Xu, Ting</creatorcontrib><creatorcontrib>Zhang, Juechao</creatorcontrib><creatorcontrib>Shang, Xin</creatorcontrib><creatorcontrib>Luo, Jixian</creatorcontrib><creatorcontrib>Chen, Liang</creatorcontrib><creatorcontrib>Ba, Xueqing</creatorcontrib><creatorcontrib>Zeng, Xianlu</creatorcontrib><title>c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show that c-Abl kinase is activated by beta(2) integrin engagement and is required for beta(2) integrin-dependent neutrophil sustained adhesion and spreading. The expression of beta(2) integrin on neutrophils induced by TNF-alpha is not affected by c-Abl kinase inhibitor STI571, suggesting that c-Abl kinase is not involved in TNF-alpha-induced integrin activation. The recruitment of c-Abl kinase to beta(2) integrin is dependent on talin head domain, which constitutively interacts with beta(2) integrin cytoplasmic domain. After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav. The SH3 domain of c-Abl kinase is involved in its interaction with talin and Vav. Thus, c-Abl kinase plays an essential role in the activation of Vav induced by beta(2) integrin ligation and in regulating neutrophil-sustained adhesion and spreading.</description><subject>CD18 Antigens - metabolism</subject><subject>CD18 Antigens - physiology</subject><subject>Cell Adhesion - immunology</subject><subject>Cytoplasm - enzymology</subject><subject>Cytoplasm - immunology</subject><subject>Cytoplasm - metabolism</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Neutrophil Activation - immunology</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - enzymology</subject><subject>Neutrophils - immunology</subject><subject>Protein Structure, Tertiary</subject><subject>Proto-Oncogene Proteins c-abl - metabolism</subject><subject>Proto-Oncogene Proteins c-abl - physiology</subject><subject>Signal Transduction - immunology</subject><subject>Talin - physiology</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1jztPwzAUhS0kREthZ0Ke2FLsa_s6HquKR6VKDLBHTuNQl8RJ7Xjg3xMJmM5wPp0HIXecrSWT5vHk-z6HoVuzkgECvyBLrhQrEBkuyHVKJ8YYMpBXZMENCAnAl2R3KDZ1R798sMlRn2h05-yja2g7RFq7yVKgPkzuM_pQ9K7xdprN4PIUh_HoO2qbo0t-CDfksrVdcrd_uiLvz08f29di__ay2272xagkL9TcWopWG8u5hIZBaYy0AhQqaFE0KByWoBFkqQRXUnPNoVFgUNSlbsWKPPymjnE4Z5emqvfp4LrOBjfkVCEaBVrqGbz_A3M9z67G6Hsbv6v_6-IHfbFXxw</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Cui, Lingling</creator><creator>Chen, Cuixia</creator><creator>Xu, Ting</creator><creator>Zhang, Juechao</creator><creator>Shang, Xin</creator><creator>Luo, Jixian</creator><creator>Chen, Liang</creator><creator>Ba, Xueqing</creator><creator>Zeng, Xianlu</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20090301</creationdate><title>c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion</title><author>Cui, Lingling ; Chen, Cuixia ; Xu, Ting ; Zhang, Juechao ; Shang, Xin ; Luo, Jixian ; Chen, Liang ; Ba, Xueqing ; Zeng, Xianlu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p541-522183f79a1142d028994a325652f63d63e682762485315471712d52963b87f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>CD18 Antigens - metabolism</topic><topic>CD18 Antigens - physiology</topic><topic>Cell Adhesion - immunology</topic><topic>Cytoplasm - enzymology</topic><topic>Cytoplasm - immunology</topic><topic>Cytoplasm - metabolism</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Neutrophil Activation - immunology</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - enzymology</topic><topic>Neutrophils - immunology</topic><topic>Protein Structure, Tertiary</topic><topic>Proto-Oncogene Proteins c-abl - metabolism</topic><topic>Proto-Oncogene Proteins c-abl - physiology</topic><topic>Signal Transduction - immunology</topic><topic>Talin - physiology</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cui, Lingling</creatorcontrib><creatorcontrib>Chen, Cuixia</creatorcontrib><creatorcontrib>Xu, Ting</creatorcontrib><creatorcontrib>Zhang, Juechao</creatorcontrib><creatorcontrib>Shang, Xin</creatorcontrib><creatorcontrib>Luo, Jixian</creatorcontrib><creatorcontrib>Chen, Liang</creatorcontrib><creatorcontrib>Ba, Xueqing</creatorcontrib><creatorcontrib>Zeng, Xianlu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cui, Lingling</au><au>Chen, Cuixia</au><au>Xu, Ting</au><au>Zhang, Juechao</au><au>Shang, Xin</au><au>Luo, Jixian</au><au>Chen, Liang</au><au>Ba, Xueqing</au><au>Zeng, Xianlu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>182</volume><issue>5</issue><spage>3233</spage><epage>3242</epage><pages>3233-3242</pages><eissn>1550-6606</eissn><abstract>Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show that c-Abl kinase is activated by beta(2) integrin engagement and is required for beta(2) integrin-dependent neutrophil sustained adhesion and spreading. The expression of beta(2) integrin on neutrophils induced by TNF-alpha is not affected by c-Abl kinase inhibitor STI571, suggesting that c-Abl kinase is not involved in TNF-alpha-induced integrin activation. The recruitment of c-Abl kinase to beta(2) integrin is dependent on talin head domain, which constitutively interacts with beta(2) integrin cytoplasmic domain. After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav. The SH3 domain of c-Abl kinase is involved in its interaction with talin and Vav. Thus, c-Abl kinase plays an essential role in the activation of Vav induced by beta(2) integrin ligation and in regulating neutrophil-sustained adhesion and spreading.</abstract><cop>United States</cop><pmid>19234221</pmid><doi>10.4049/jimmunol.0802621</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | EISSN: 1550-6606 |
| ispartof | The Journal of immunology (1950), 2009-03, Vol.182 (5), p.3233-3242 |
| issn | 1550-6606 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_66952747 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | CD18 Antigens - metabolism CD18 Antigens - physiology Cell Adhesion - immunology Cytoplasm - enzymology Cytoplasm - immunology Cytoplasm - metabolism HL-60 Cells Humans Neutrophil Activation - immunology Neutrophils - cytology Neutrophils - enzymology Neutrophils - immunology Protein Structure, Tertiary Proto-Oncogene Proteins c-abl - metabolism Proto-Oncogene Proteins c-abl - physiology Signal Transduction - immunology Talin - physiology Tumor Necrosis Factor-alpha - physiology |
| title | c-Abl kinase is required for beta 2 integrin-mediated neutrophil adhesion |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T21%3A08%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=c-Abl%20kinase%20is%20required%20for%20beta%202%20integrin-mediated%20neutrophil%20adhesion&rft.jtitle=The%20Journal%20of%20immunology%20(1950)&rft.au=Cui,%20Lingling&rft.date=2009-03-01&rft.volume=182&rft.issue=5&rft.spage=3233&rft.epage=3242&rft.pages=3233-3242&rft.eissn=1550-6606&rft_id=info:doi/10.4049/jimmunol.0802621&rft_dat=%3Cproquest_pubme%3E66952747%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=66952747&rft_id=info:pmid/19234221&rfr_iscdi=true |