Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1
Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tum...
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Veröffentlicht in: | Medical molecular morphology 2013-03, Vol.46 (1), p.14-19 |
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description | Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-
S
-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation. |
doi_str_mv | 10.1007/s00795-012-0002-z |
format | Article |
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S
-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.</description><identifier>ISSN: 1860-1480</identifier><identifier>EISSN: 1860-1499</identifier><identifier>DOI: 10.1007/s00795-012-0002-z</identifier><identifier>PMID: 23325550</identifier><identifier>CODEN: MELMEJ</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>Adenocarcinoma ; Adenocarcinoma - metabolism ; Anatomy ; Biological assays ; Catalytic Domain - genetics ; Cell Line, Tumor ; Colonic Neoplasms - metabolism ; Colorectal cancer ; Deoxyribonucleic acid ; DNA ; DNA-Activated Protein Kinase - genetics ; DNA-Activated Protein Kinase - metabolism ; Fluorescent Antibody Technique ; Gene Expression Regulation, Neoplastic - genetics ; Glutathione Transferase ; Humans ; Immunoprecipitation ; Kinases ; Lymphocytes ; Lymphoid Enhancer-Binding Factor 1 - metabolism ; Mass Spectrometry ; Medicine ; Medicine & Public Health ; Molecular Medicine ; Original Paper ; Pathology ; Proteins ; Wnt Signaling Pathway - genetics</subject><ispartof>Medical molecular morphology, 2013-03, Vol.46 (1), p.14-19</ispartof><rights>The Japanese Society for Clinical Molecular Morphology 2012</rights><rights>The Japanese Society for Clinical Molecular Morphology 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-ff947d38772664279116fd84a5ceab6e68fff2ab1ed5bd8ff9884db964b72fb03</citedby><cites>FETCH-LOGICAL-c524t-ff947d38772664279116fd84a5ceab6e68fff2ab1ed5bd8ff9884db964b72fb03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00795-012-0002-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00795-012-0002-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23325550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shimomura, Atsushi</creatorcontrib><creatorcontrib>Takasaki, Akihiko</creatorcontrib><creatorcontrib>Nomura, Ryuji</creatorcontrib><creatorcontrib>Hayashi, Nobuhiro</creatorcontrib><creatorcontrib>Senda, Takao</creatorcontrib><title>Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1</title><title>Medical molecular morphology</title><addtitle>Med Mol Morphol</addtitle><addtitle>Med Mol Morphol</addtitle><description>Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-
S
-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - metabolism</subject><subject>Anatomy</subject><subject>Biological assays</subject><subject>Catalytic Domain - genetics</subject><subject>Cell Line, Tumor</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal cancer</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA-Activated Protein Kinase - genetics</subject><subject>DNA-Activated Protein Kinase - metabolism</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Glutathione Transferase</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Kinases</subject><subject>Lymphocytes</subject><subject>Lymphoid Enhancer-Binding Factor 1 - metabolism</subject><subject>Mass Spectrometry</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular Medicine</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Proteins</subject><subject>Wnt Signaling Pathway - genetics</subject><issn>1860-1480</issn><issn>1860-1499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkUtrFjEUhkNRev8BbiTQjZvRJDOTy7JUrYWiG7sOmcxJmzpfMk0ywteNf92MXy0iCG5yO895wuFF6BUlbykh4l2ui-obQllDCGHN4x46pJKThnZKvXg-S3KAjnK-J6QVnPX76IC1Lev7nhyiH1cjhOKdt6b4GHB0-P3n82aEGcJawXOKBXzA33wwGXDFzLQt3uK8DEvwBZuMDQ7xO0zYhwLJ2F-i2aQSIK3CabuZ76LdFsAQ7kyw9dlVLCZMT9BLZ6YMp0_7Mbr5-OHrxafm-svl1cX5dWN71pXGOdWJsZVCMM47JhSl3I2yM70FM3Dg0jnHzEBh7IexXpSU3Tgo3g2CuYG0x-jNzlvneVggF73x2cI0mQBxyZq2rJVVquh_oFQSxalgFT37C72PSwp1kJUSopWSqUrRHWVTzDmB03PyG5O2mhK9Bql3QeoapF6D1I-15_WTeRk2MD53_E6uAmwH5FoKt5D--Pqf1p_qwapf</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Shimomura, Atsushi</creator><creator>Takasaki, Akihiko</creator><creator>Nomura, Ryuji</creator><creator>Hayashi, Nobuhiro</creator><creator>Senda, Takao</creator><general>Springer Japan</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>7T5</scope><scope>7TM</scope><scope>H94</scope></search><sort><creationdate>20130301</creationdate><title>Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1</title><author>Shimomura, Atsushi ; Takasaki, Akihiko ; Nomura, Ryuji ; Hayashi, Nobuhiro ; Senda, Takao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-ff947d38772664279116fd84a5ceab6e68fff2ab1ed5bd8ff9884db964b72fb03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - metabolism</topic><topic>Anatomy</topic><topic>Biological assays</topic><topic>Catalytic Domain - genetics</topic><topic>Cell Line, Tumor</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colorectal cancer</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA-Activated Protein Kinase - genetics</topic><topic>DNA-Activated Protein Kinase - metabolism</topic><topic>Fluorescent Antibody Technique</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Glutathione Transferase</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Kinases</topic><topic>Lymphocytes</topic><topic>Lymphoid Enhancer-Binding Factor 1 - metabolism</topic><topic>Mass Spectrometry</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular Medicine</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Proteins</topic><topic>Wnt Signaling Pathway - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimomura, Atsushi</creatorcontrib><creatorcontrib>Takasaki, Akihiko</creatorcontrib><creatorcontrib>Nomura, Ryuji</creatorcontrib><creatorcontrib>Hayashi, Nobuhiro</creatorcontrib><creatorcontrib>Senda, Takao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Medical molecular morphology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimomura, Atsushi</au><au>Takasaki, Akihiko</au><au>Nomura, Ryuji</au><au>Hayashi, Nobuhiro</au><au>Senda, Takao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1</atitle><jtitle>Medical molecular morphology</jtitle><stitle>Med Mol Morphol</stitle><addtitle>Med Mol Morphol</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>46</volume><issue>1</issue><spage>14</spage><epage>19</epage><pages>14-19</pages><issn>1860-1480</issn><eissn>1860-1499</eissn><coden>MELMEJ</coden><abstract>Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-
S
-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>23325550</pmid><doi>10.1007/s00795-012-0002-z</doi><tpages>6</tpages></addata></record> |
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subjects | Adenocarcinoma Adenocarcinoma - metabolism Anatomy Biological assays Catalytic Domain - genetics Cell Line, Tumor Colonic Neoplasms - metabolism Colorectal cancer Deoxyribonucleic acid DNA DNA-Activated Protein Kinase - genetics DNA-Activated Protein Kinase - metabolism Fluorescent Antibody Technique Gene Expression Regulation, Neoplastic - genetics Glutathione Transferase Humans Immunoprecipitation Kinases Lymphocytes Lymphoid Enhancer-Binding Factor 1 - metabolism Mass Spectrometry Medicine Medicine & Public Health Molecular Medicine Original Paper Pathology Proteins Wnt Signaling Pathway - genetics |
title | Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1 |
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