Loading…
MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1
Cell adhesion molecules (CAMs) are involved in a variety of pathologies including cancer, inflammation, pathogenic infections and autoimmune disease. In particular, VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. Therefore, we attempted to e...
Saved in:
Published in: | Cellular signalling 2012-04, Vol.24 (4), p.866-872 |
---|---|
Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73 |
---|---|
cites | cdi_FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73 |
container_end_page | 872 |
container_issue | 4 |
container_start_page | 866 |
container_title | Cellular signalling |
container_volume | 24 |
creator | Nizamutdinova, Irina Tsoy Kim, Young Min Lee, Jae Heun Chang, Ki Churl Kim, Hye Jung |
description | Cell adhesion molecules (CAMs) are involved in a variety of pathologies including cancer, inflammation, pathogenic infections and autoimmune disease. In particular, VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. Therefore, we attempted to elucidate differential mechanisms that regulate VCAM-1 and ICAM-1 expressions. Down-regulation of JNK by a specific inhibitor (SP600125) or dominant negative (DN) JNK1 plasmid enhanced TNF-α-induced VCAM-1 but not ICAM-1 expression. Moreover, transfection with a JNK1-overexpressing vector resulted in the inhibition of VCAM-1 expression stimulated by TNF-α in HUVECs, suggesting that JNK negatively regulates TNF-α-induced VCAM-1 expression in endothelial cells (ECs). Next, we investigated whether JNK signaling affects IRF-1 and/or GATA6, which are transcription factors that mediate TNF-α induction of VCAM-1 but not ICAM-1. The DN-JNK1 plasmid-transfected cells enhanced TNF-α up-regulation of IRF-1 whereas JNK1-overexpressing cells displayed down-regulation; however, neither DN-JNK1 transfection nor JNK1 overexpression affected GATA6 protein levels in the nuclear fraction. Chromatin immunoprecipitation (ChIP) assay confirmed that the inhibition of JNK by DN-JNK1 transfection increases the binding of IRF-1 to the VCAM-1 promoter whereas the overexpression of JNK1 inhibits IRF-1 binding to the VCAM-1 promoter. However, neither DN-JNK1 nor JNK1 overexpression altered GATA6 affinity for the VCAM-1 promoter region. We also examined whether MKP-7 affects ICAM-1 or VCAM-1 by regulating JNK. TNF-α-induced phosphor-JNK levels increased after 5min, peaked at 10min, and decreased after 30min. Interestingly, MKP-7 protein levels increased after 30min, when phosphor-JNK induction by TNF-α was decreased. In addition, silencing MKP-7 with specific siRNA resulted in an increase in phosphor-JNK and inhibited the expression of VCAM-1 but not ICAM-1. Moreover, silencing MKP-7 caused the down-regulation of IRF-1 protein levels and binding to the VCAM-1 promoter. Thus, we suggest that MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.
► VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. ► The existence of IRF-1 and GATA functional transcription factor binding motifs in the VCAM-1 gene promoter region distinguishes VCAM-1 from other CAMs. ► We discovered that s |
doi_str_mv | 10.1016/j.cellsig.2011.12.002 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_918933203</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0898656811003809</els_id><sourcerecordid>918933203</sourcerecordid><originalsourceid>FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73</originalsourceid><addsrcrecordid>eNqFkFFPwjAQxxujEUQ_gqZvvrDZa9exPRlCRBFQY9TXpttuUDI2bDei394R0FeTSy65_P53uR8hl8B8YBDerPwUi8KZhc8ZgA_cZ4wfkS5EA-GJGMQx6bIojrxQhlGHnDm3YgwkC_kp6XAOEZfAu2Q-n754gz7VtMSFrs0WqcVFU-i6srTK6ePTtP87QUc_RsO5BxS_NhadM1VJ66WtmsWSTl7HHpyTk1wXDi8OvUfex3dvowdv9nw_GQ1nXhoIVntS6wSDLABkguc8kQOWiRAhztsKOCAEEoJEQxpwqUUUJsjiQMep1DIM84Hokev93o2tPht0tVobt_OhS6wap2KIYiE4Ey0p92RqK-cs5mpjzVrbbwVM7USqlTqIVDuRCrhqRba5q8OFJllj9pf6NdcCt3sA2z-3Bq1yqcEyxcxYTGuVVeafEz-eIIPI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>918933203</pqid></control><display><type>article</type><title>MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1</title><source>ScienceDirect Journals</source><creator>Nizamutdinova, Irina Tsoy ; Kim, Young Min ; Lee, Jae Heun ; Chang, Ki Churl ; Kim, Hye Jung</creator><creatorcontrib>Nizamutdinova, Irina Tsoy ; Kim, Young Min ; Lee, Jae Heun ; Chang, Ki Churl ; Kim, Hye Jung</creatorcontrib><description>Cell adhesion molecules (CAMs) are involved in a variety of pathologies including cancer, inflammation, pathogenic infections and autoimmune disease. In particular, VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. Therefore, we attempted to elucidate differential mechanisms that regulate VCAM-1 and ICAM-1 expressions. Down-regulation of JNK by a specific inhibitor (SP600125) or dominant negative (DN) JNK1 plasmid enhanced TNF-α-induced VCAM-1 but not ICAM-1 expression. Moreover, transfection with a JNK1-overexpressing vector resulted in the inhibition of VCAM-1 expression stimulated by TNF-α in HUVECs, suggesting that JNK negatively regulates TNF-α-induced VCAM-1 expression in endothelial cells (ECs). Next, we investigated whether JNK signaling affects IRF-1 and/or GATA6, which are transcription factors that mediate TNF-α induction of VCAM-1 but not ICAM-1. The DN-JNK1 plasmid-transfected cells enhanced TNF-α up-regulation of IRF-1 whereas JNK1-overexpressing cells displayed down-regulation; however, neither DN-JNK1 transfection nor JNK1 overexpression affected GATA6 protein levels in the nuclear fraction. Chromatin immunoprecipitation (ChIP) assay confirmed that the inhibition of JNK by DN-JNK1 transfection increases the binding of IRF-1 to the VCAM-1 promoter whereas the overexpression of JNK1 inhibits IRF-1 binding to the VCAM-1 promoter. However, neither DN-JNK1 nor JNK1 overexpression altered GATA6 affinity for the VCAM-1 promoter region. We also examined whether MKP-7 affects ICAM-1 or VCAM-1 by regulating JNK. TNF-α-induced phosphor-JNK levels increased after 5min, peaked at 10min, and decreased after 30min. Interestingly, MKP-7 protein levels increased after 30min, when phosphor-JNK induction by TNF-α was decreased. In addition, silencing MKP-7 with specific siRNA resulted in an increase in phosphor-JNK and inhibited the expression of VCAM-1 but not ICAM-1. Moreover, silencing MKP-7 caused the down-regulation of IRF-1 protein levels and binding to the VCAM-1 promoter. Thus, we suggest that MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.
► VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. ► The existence of IRF-1 and GATA functional transcription factor binding motifs in the VCAM-1 gene promoter region distinguishes VCAM-1 from other CAMs. ► We discovered that specific inhibition of JNK1 in endothelial cells enhances TNF-α-mediated VCAM-1 induction. ► JNK activation by TNF-α is negatively regulated by MKP-7 in endothelial cell, and down-regulation of JNK1 leads to up-regulation of IRF-1, which is important in activation of VCAM-1, but not ICAM-1.</description><identifier>ISSN: 0898-6568</identifier><identifier>EISSN: 1873-3913</identifier><identifier>DOI: 10.1016/j.cellsig.2011.12.002</identifier><identifier>PMID: 22182512</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Chromatin Immunoprecipitation ; Dual-Specificity Phosphatases - genetics ; Dual-Specificity Phosphatases - metabolism ; GATA6 ; GATA6 Transcription Factor - genetics ; GATA6 Transcription Factor - metabolism ; Gene Expression Regulation ; Genes, Reporter ; Human Umbilical Vein Endothelial Cells ; Humans ; ICAM-1 ; Interferon Regulatory Factor-1 - genetics ; Interferon Regulatory Factor-1 - metabolism ; IRF-1 ; JNK ; Luciferases ; MAP Kinase Kinase 4 - antagonists & inhibitors ; MAP Kinase Kinase 4 - genetics ; MAP Kinase Kinase 4 - metabolism ; Mitogen-Activated Protein Kinase Phosphatases - genetics ; Mitogen-Activated Protein Kinase Phosphatases - metabolism ; MKP-7 ; Plasmids ; Protein Kinase Inhibitors - pharmacology ; Signal Transduction - genetics ; Transfection ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism ; VCAM-1</subject><ispartof>Cellular signalling, 2012-04, Vol.24 (4), p.866-872</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73</citedby><cites>FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22182512$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nizamutdinova, Irina Tsoy</creatorcontrib><creatorcontrib>Kim, Young Min</creatorcontrib><creatorcontrib>Lee, Jae Heun</creatorcontrib><creatorcontrib>Chang, Ki Churl</creatorcontrib><creatorcontrib>Kim, Hye Jung</creatorcontrib><title>MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1</title><title>Cellular signalling</title><addtitle>Cell Signal</addtitle><description>Cell adhesion molecules (CAMs) are involved in a variety of pathologies including cancer, inflammation, pathogenic infections and autoimmune disease. In particular, VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. Therefore, we attempted to elucidate differential mechanisms that regulate VCAM-1 and ICAM-1 expressions. Down-regulation of JNK by a specific inhibitor (SP600125) or dominant negative (DN) JNK1 plasmid enhanced TNF-α-induced VCAM-1 but not ICAM-1 expression. Moreover, transfection with a JNK1-overexpressing vector resulted in the inhibition of VCAM-1 expression stimulated by TNF-α in HUVECs, suggesting that JNK negatively regulates TNF-α-induced VCAM-1 expression in endothelial cells (ECs). Next, we investigated whether JNK signaling affects IRF-1 and/or GATA6, which are transcription factors that mediate TNF-α induction of VCAM-1 but not ICAM-1. The DN-JNK1 plasmid-transfected cells enhanced TNF-α up-regulation of IRF-1 whereas JNK1-overexpressing cells displayed down-regulation; however, neither DN-JNK1 transfection nor JNK1 overexpression affected GATA6 protein levels in the nuclear fraction. Chromatin immunoprecipitation (ChIP) assay confirmed that the inhibition of JNK by DN-JNK1 transfection increases the binding of IRF-1 to the VCAM-1 promoter whereas the overexpression of JNK1 inhibits IRF-1 binding to the VCAM-1 promoter. However, neither DN-JNK1 nor JNK1 overexpression altered GATA6 affinity for the VCAM-1 promoter region. We also examined whether MKP-7 affects ICAM-1 or VCAM-1 by regulating JNK. TNF-α-induced phosphor-JNK levels increased after 5min, peaked at 10min, and decreased after 30min. Interestingly, MKP-7 protein levels increased after 30min, when phosphor-JNK induction by TNF-α was decreased. In addition, silencing MKP-7 with specific siRNA resulted in an increase in phosphor-JNK and inhibited the expression of VCAM-1 but not ICAM-1. Moreover, silencing MKP-7 caused the down-regulation of IRF-1 protein levels and binding to the VCAM-1 promoter. Thus, we suggest that MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.
► VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. ► The existence of IRF-1 and GATA functional transcription factor binding motifs in the VCAM-1 gene promoter region distinguishes VCAM-1 from other CAMs. ► We discovered that specific inhibition of JNK1 in endothelial cells enhances TNF-α-mediated VCAM-1 induction. ► JNK activation by TNF-α is negatively regulated by MKP-7 in endothelial cell, and down-regulation of JNK1 leads to up-regulation of IRF-1, which is important in activation of VCAM-1, but not ICAM-1.</description><subject>Chromatin Immunoprecipitation</subject><subject>Dual-Specificity Phosphatases - genetics</subject><subject>Dual-Specificity Phosphatases - metabolism</subject><subject>GATA6</subject><subject>GATA6 Transcription Factor - genetics</subject><subject>GATA6 Transcription Factor - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>ICAM-1</subject><subject>Interferon Regulatory Factor-1 - genetics</subject><subject>Interferon Regulatory Factor-1 - metabolism</subject><subject>IRF-1</subject><subject>JNK</subject><subject>Luciferases</subject><subject>MAP Kinase Kinase 4 - antagonists & inhibitors</subject><subject>MAP Kinase Kinase 4 - genetics</subject><subject>MAP Kinase Kinase 4 - metabolism</subject><subject>Mitogen-Activated Protein Kinase Phosphatases - genetics</subject><subject>Mitogen-Activated Protein Kinase Phosphatases - metabolism</subject><subject>MKP-7</subject><subject>Plasmids</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Signal Transduction - genetics</subject><subject>Transfection</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>VCAM-1</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqFkFFPwjAQxxujEUQ_gqZvvrDZa9exPRlCRBFQY9TXpttuUDI2bDei394R0FeTSy65_P53uR8hl8B8YBDerPwUi8KZhc8ZgA_cZ4wfkS5EA-GJGMQx6bIojrxQhlGHnDm3YgwkC_kp6XAOEZfAu2Q-n754gz7VtMSFrs0WqcVFU-i6srTK6ePTtP87QUc_RsO5BxS_NhadM1VJ66WtmsWSTl7HHpyTk1wXDi8OvUfex3dvowdv9nw_GQ1nXhoIVntS6wSDLABkguc8kQOWiRAhztsKOCAEEoJEQxpwqUUUJsjiQMep1DIM84Hokev93o2tPht0tVobt_OhS6wap2KIYiE4Ey0p92RqK-cs5mpjzVrbbwVM7USqlTqIVDuRCrhqRba5q8OFJllj9pf6NdcCt3sA2z-3Bq1yqcEyxcxYTGuVVeafEz-eIIPI</recordid><startdate>201204</startdate><enddate>201204</enddate><creator>Nizamutdinova, Irina Tsoy</creator><creator>Kim, Young Min</creator><creator>Lee, Jae Heun</creator><creator>Chang, Ki Churl</creator><creator>Kim, Hye Jung</creator><general>Elsevier Inc</general><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>201204</creationdate><title>MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1</title><author>Nizamutdinova, Irina Tsoy ; Kim, Young Min ; Lee, Jae Heun ; Chang, Ki Churl ; Kim, Hye Jung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Chromatin Immunoprecipitation</topic><topic>Dual-Specificity Phosphatases - genetics</topic><topic>Dual-Specificity Phosphatases - metabolism</topic><topic>GATA6</topic><topic>GATA6 Transcription Factor - genetics</topic><topic>GATA6 Transcription Factor - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>ICAM-1</topic><topic>Interferon Regulatory Factor-1 - genetics</topic><topic>Interferon Regulatory Factor-1 - metabolism</topic><topic>IRF-1</topic><topic>JNK</topic><topic>Luciferases</topic><topic>MAP Kinase Kinase 4 - antagonists & inhibitors</topic><topic>MAP Kinase Kinase 4 - genetics</topic><topic>MAP Kinase Kinase 4 - metabolism</topic><topic>Mitogen-Activated Protein Kinase Phosphatases - genetics</topic><topic>Mitogen-Activated Protein Kinase Phosphatases - metabolism</topic><topic>MKP-7</topic><topic>Plasmids</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Signal Transduction - genetics</topic><topic>Transfection</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>VCAM-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nizamutdinova, Irina Tsoy</creatorcontrib><creatorcontrib>Kim, Young Min</creatorcontrib><creatorcontrib>Lee, Jae Heun</creatorcontrib><creatorcontrib>Chang, Ki Churl</creatorcontrib><creatorcontrib>Kim, Hye Jung</creatorcontrib><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>Cellular signalling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nizamutdinova, Irina Tsoy</au><au>Kim, Young Min</au><au>Lee, Jae Heun</au><au>Chang, Ki Churl</au><au>Kim, Hye Jung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1</atitle><jtitle>Cellular signalling</jtitle><addtitle>Cell Signal</addtitle><date>2012-04</date><risdate>2012</risdate><volume>24</volume><issue>4</issue><spage>866</spage><epage>872</epage><pages>866-872</pages><issn>0898-6568</issn><eissn>1873-3913</eissn><abstract>Cell adhesion molecules (CAMs) are involved in a variety of pathologies including cancer, inflammation, pathogenic infections and autoimmune disease. In particular, VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. Therefore, we attempted to elucidate differential mechanisms that regulate VCAM-1 and ICAM-1 expressions. Down-regulation of JNK by a specific inhibitor (SP600125) or dominant negative (DN) JNK1 plasmid enhanced TNF-α-induced VCAM-1 but not ICAM-1 expression. Moreover, transfection with a JNK1-overexpressing vector resulted in the inhibition of VCAM-1 expression stimulated by TNF-α in HUVECs, suggesting that JNK negatively regulates TNF-α-induced VCAM-1 expression in endothelial cells (ECs). Next, we investigated whether JNK signaling affects IRF-1 and/or GATA6, which are transcription factors that mediate TNF-α induction of VCAM-1 but not ICAM-1. The DN-JNK1 plasmid-transfected cells enhanced TNF-α up-regulation of IRF-1 whereas JNK1-overexpressing cells displayed down-regulation; however, neither DN-JNK1 transfection nor JNK1 overexpression affected GATA6 protein levels in the nuclear fraction. Chromatin immunoprecipitation (ChIP) assay confirmed that the inhibition of JNK by DN-JNK1 transfection increases the binding of IRF-1 to the VCAM-1 promoter whereas the overexpression of JNK1 inhibits IRF-1 binding to the VCAM-1 promoter. However, neither DN-JNK1 nor JNK1 overexpression altered GATA6 affinity for the VCAM-1 promoter region. We also examined whether MKP-7 affects ICAM-1 or VCAM-1 by regulating JNK. TNF-α-induced phosphor-JNK levels increased after 5min, peaked at 10min, and decreased after 30min. Interestingly, MKP-7 protein levels increased after 30min, when phosphor-JNK induction by TNF-α was decreased. In addition, silencing MKP-7 with specific siRNA resulted in an increase in phosphor-JNK and inhibited the expression of VCAM-1 but not ICAM-1. Moreover, silencing MKP-7 caused the down-regulation of IRF-1 protein levels and binding to the VCAM-1 promoter. Thus, we suggest that MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.
► VCAM-1, rather than ICAM-1, plays a major role in the initiation of atherosclerosis and tumor progression. ► The existence of IRF-1 and GATA functional transcription factor binding motifs in the VCAM-1 gene promoter region distinguishes VCAM-1 from other CAMs. ► We discovered that specific inhibition of JNK1 in endothelial cells enhances TNF-α-mediated VCAM-1 induction. ► JNK activation by TNF-α is negatively regulated by MKP-7 in endothelial cell, and down-regulation of JNK1 leads to up-regulation of IRF-1, which is important in activation of VCAM-1, but not ICAM-1.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>22182512</pmid><doi>10.1016/j.cellsig.2011.12.002</doi><tpages>7</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0898-6568 |
ispartof | Cellular signalling, 2012-04, Vol.24 (4), p.866-872 |
issn | 0898-6568 1873-3913 |
language | eng |
recordid | cdi_proquest_miscellaneous_918933203 |
source | ScienceDirect Journals |
subjects | Chromatin Immunoprecipitation Dual-Specificity Phosphatases - genetics Dual-Specificity Phosphatases - metabolism GATA6 GATA6 Transcription Factor - genetics GATA6 Transcription Factor - metabolism Gene Expression Regulation Genes, Reporter Human Umbilical Vein Endothelial Cells Humans ICAM-1 Interferon Regulatory Factor-1 - genetics Interferon Regulatory Factor-1 - metabolism IRF-1 JNK Luciferases MAP Kinase Kinase 4 - antagonists & inhibitors MAP Kinase Kinase 4 - genetics MAP Kinase Kinase 4 - metabolism Mitogen-Activated Protein Kinase Phosphatases - genetics Mitogen-Activated Protein Kinase Phosphatases - metabolism MKP-7 Plasmids Protein Kinase Inhibitors - pharmacology Signal Transduction - genetics Transfection Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism VCAM-1 |
title | MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1 |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T05%3A57%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MKP-7,%20a%20negative%20regulator%20of%20JNK,%20regulates%20VCAM-1%20expression%20through%20IRF-1&rft.jtitle=Cellular%20signalling&rft.au=Nizamutdinova,%20Irina%20Tsoy&rft.date=2012-04&rft.volume=24&rft.issue=4&rft.spage=866&rft.epage=872&rft.pages=866-872&rft.issn=0898-6568&rft.eissn=1873-3913&rft_id=info:doi/10.1016/j.cellsig.2011.12.002&rft_dat=%3Cproquest_cross%3E918933203%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c430t-5aabe4d41e032f2b570d36e19f19f421e14514ba1c425a386be094a9c5a566f73%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=918933203&rft_id=info:pmid/22182512&rfr_iscdi=true |