Regulation of the Nuclear Factor of Activated T Cells in Stably Transfected Jurkat Cell Clones
Two Jurkat cell clones have been stably transfected with a reporter vector for the nuclear factor of activated T cells (NFAT). Upon stimulation, they express high levels of secreted heat stable placental alkaline phosphatase. With these clones, we demonstrated that NFAT activation induced by phorbol...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1996-02, Vol.219 (1), p.96-99 |
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| creator | Li, Wei Handschumacher, Robert E. |
| description | Two Jurkat cell clones have been stably transfected with a reporter vector for the nuclear factor of activated T cells (NFAT). Upon stimulation, they express high levels of secreted heat stable placental alkaline phosphatase. With these clones, we demonstrated that NFAT activation induced by phorbol 12-myristate 13-acetate and ionomycin was inhibited by both cyclosporin A (CsA) (IC50= 8 nM) and FK506 (IC50= 160 pM), presumably by inhibition of calcineurin activity. Selective phosphatase inhibitors for protein phophatase 1 (PP1) and 2A (PP2A) that do not inhibit calcineurin, such as okadaic acid and calyculin A, also inhibited NFAT activation with IC50s of 87 nM and 4 nM, respectively, suggesting that okadaic acid and related inhibitiors may block NFAT activation through the inhibition of PP1, instead of PP2A. NFAT activation was also inhibited by agents that increase cAMP concentrations such as dibutyryl cAMP, forskolin and prostaglandin E2. These stable Jurkat cell clones proved a convenient and sensitive tool to study NFAT regulation. |
| doi_str_mv | 10.1006/bbrc.1996.0187 |
| format | Article |
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Upon stimulation, they express high levels of secreted heat stable placental alkaline phosphatase. With these clones, we demonstrated that NFAT activation induced by phorbol 12-myristate 13-acetate and ionomycin was inhibited by both cyclosporin A (CsA) (IC50= 8 nM) and FK506 (IC50= 160 pM), presumably by inhibition of calcineurin activity. Selective phosphatase inhibitors for protein phophatase 1 (PP1) and 2A (PP2A) that do not inhibit calcineurin, such as okadaic acid and calyculin A, also inhibited NFAT activation with IC50s of 87 nM and 4 nM, respectively, suggesting that okadaic acid and related inhibitiors may block NFAT activation through the inhibition of PP1, instead of PP2A. NFAT activation was also inhibited by agents that increase cAMP concentrations such as dibutyryl cAMP, forskolin and prostaglandin E2. These stable Jurkat cell clones proved a convenient and sensitive tool to study NFAT regulation.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.1996.0187</identifier><identifier>PMID: 8619834</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alkaline Phosphatase - biosynthesis ; Bucladesine - pharmacology ; Clone Cells ; Colforsin - pharmacology ; Cyclosporine - pharmacology ; Dinoprostone - pharmacology ; DNA-Binding Proteins - biosynthesis ; DNA-Binding Proteins - physiology ; Enzyme Inhibitors - pharmacology ; Ethers, Cyclic - pharmacology ; Female ; Humans ; Immunosuppressive Agents - pharmacology ; Kinetics ; Lymphocyte Activation ; NFATC Transcription Factors ; Nuclear Proteins ; Okadaic Acid ; Oxazoles - pharmacology ; Phosphoprotein Phosphatases - antagonists & inhibitors ; Placenta ; Pregnancy ; Protein Phosphatase 1 ; Recombinant Proteins - biosynthesis ; Recombinant Proteins - metabolism ; T-Lymphocytes - drug effects ; T-Lymphocytes - immunology ; T-Lymphocytes - physiology ; Tacrolimus - pharmacology ; Tetradecanoylphorbol Acetate - pharmacology ; Transcription Factors - biosynthesis ; Transcription Factors - physiology ; Transfection ; Tumor Cells, Cultured</subject><ispartof>Biochemical and biophysical research communications, 1996-02, Vol.219 (1), p.96-99</ispartof><rights>1996 Academic Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-76b0acd94111078f13007485d90f69cb93f3f5f5be6e9f496ddee00c394006b93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.1996.0187$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8619834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Handschumacher, Robert E.</creatorcontrib><title>Regulation of the Nuclear Factor of Activated T Cells in Stably Transfected Jurkat Cell Clones</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Two Jurkat cell clones have been stably transfected with a reporter vector for the nuclear factor of activated T cells (NFAT). Upon stimulation, they express high levels of secreted heat stable placental alkaline phosphatase. With these clones, we demonstrated that NFAT activation induced by phorbol 12-myristate 13-acetate and ionomycin was inhibited by both cyclosporin A (CsA) (IC50= 8 nM) and FK506 (IC50= 160 pM), presumably by inhibition of calcineurin activity. Selective phosphatase inhibitors for protein phophatase 1 (PP1) and 2A (PP2A) that do not inhibit calcineurin, such as okadaic acid and calyculin A, also inhibited NFAT activation with IC50s of 87 nM and 4 nM, respectively, suggesting that okadaic acid and related inhibitiors may block NFAT activation through the inhibition of PP1, instead of PP2A. NFAT activation was also inhibited by agents that increase cAMP concentrations such as dibutyryl cAMP, forskolin and prostaglandin E2. These stable Jurkat cell clones proved a convenient and sensitive tool to study NFAT regulation.</description><subject>Alkaline Phosphatase - biosynthesis</subject><subject>Bucladesine - pharmacology</subject><subject>Clone Cells</subject><subject>Colforsin - pharmacology</subject><subject>Cyclosporine - pharmacology</subject><subject>Dinoprostone - pharmacology</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Ethers, Cyclic - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Kinetics</subject><subject>Lymphocyte Activation</subject><subject>NFATC Transcription Factors</subject><subject>Nuclear Proteins</subject><subject>Okadaic Acid</subject><subject>Oxazoles - pharmacology</subject><subject>Phosphoprotein Phosphatases - antagonists & inhibitors</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Protein Phosphatase 1</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>Recombinant Proteins - metabolism</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - physiology</subject><subject>Tacrolimus - pharmacology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Transcription Factors - biosynthesis</subject><subject>Transcription Factors - physiology</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kF9LwzAUxYMoc05ffRPyBVpv1q5tHkdx_mEo6ASfDGlyo9GuHUk62Le3dcM3ny7cc87lnh8hlwxiBpBdV5VTMeM8i4EV-REZM-AQTRmkx2QMvSOacvZ2Ss68_wJgLM34iIyKjPEiScfk_Rk_uloG2za0NTR8In3sVI3S0YVUoXXDdq6C3cqAmq5oiXXtqW3oS5BVvaMrJxtvUA3qQ-e-Zfi10LJuG_Tn5MTI2uPFYU7I6-JmVd5Fy6fb-3K-jFSS8xDlWQVSaZ4yxiAvDEsA8rSYaQ4m46riiUnMzMwqzJCblGdaIwKohKd9w16ekHh_V7nWe4dGbJxdS7cTDMTASQycxMBJDJz6wNU-sOmqNeo_-wFMrxd7Hfuvtxad8Mpio1Bb15cVurX_nf4BHJJ2og</recordid><startdate>19960206</startdate><enddate>19960206</enddate><creator>Li, Wei</creator><creator>Handschumacher, Robert E.</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></search><sort><creationdate>19960206</creationdate><title>Regulation of the Nuclear Factor of Activated T Cells in Stably Transfected Jurkat Cell Clones</title><author>Li, Wei ; Handschumacher, Robert E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-76b0acd94111078f13007485d90f69cb93f3f5f5be6e9f496ddee00c394006b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Alkaline Phosphatase - biosynthesis</topic><topic>Bucladesine - pharmacology</topic><topic>Clone Cells</topic><topic>Colforsin - pharmacology</topic><topic>Cyclosporine - pharmacology</topic><topic>Dinoprostone - pharmacology</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Ethers, Cyclic - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Kinetics</topic><topic>Lymphocyte Activation</topic><topic>NFATC Transcription Factors</topic><topic>Nuclear Proteins</topic><topic>Okadaic Acid</topic><topic>Oxazoles - pharmacology</topic><topic>Phosphoprotein Phosphatases - antagonists & inhibitors</topic><topic>Placenta</topic><topic>Pregnancy</topic><topic>Protein Phosphatase 1</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>Recombinant Proteins - metabolism</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - physiology</topic><topic>Tacrolimus - pharmacology</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Transcription Factors - biosynthesis</topic><topic>Transcription Factors - physiology</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Handschumacher, Robert E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Wei</au><au>Handschumacher, Robert E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of the Nuclear Factor of Activated T Cells in Stably Transfected Jurkat Cell Clones</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1996-02-06</date><risdate>1996</risdate><volume>219</volume><issue>1</issue><spage>96</spage><epage>99</epage><pages>96-99</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Two Jurkat cell clones have been stably transfected with a reporter vector for the nuclear factor of activated T cells (NFAT). Upon stimulation, they express high levels of secreted heat stable placental alkaline phosphatase. With these clones, we demonstrated that NFAT activation induced by phorbol 12-myristate 13-acetate and ionomycin was inhibited by both cyclosporin A (CsA) (IC50= 8 nM) and FK506 (IC50= 160 pM), presumably by inhibition of calcineurin activity. Selective phosphatase inhibitors for protein phophatase 1 (PP1) and 2A (PP2A) that do not inhibit calcineurin, such as okadaic acid and calyculin A, also inhibited NFAT activation with IC50s of 87 nM and 4 nM, respectively, suggesting that okadaic acid and related inhibitiors may block NFAT activation through the inhibition of PP1, instead of PP2A. NFAT activation was also inhibited by agents that increase cAMP concentrations such as dibutyryl cAMP, forskolin and prostaglandin E2. These stable Jurkat cell clones proved a convenient and sensitive tool to study NFAT regulation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>8619834</pmid><doi>10.1006/bbrc.1996.0187</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 1996-02, Vol.219 (1), p.96-99 |
| issn | 0006-291X 1090-2104 |
| language | eng |
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| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Alkaline Phosphatase - biosynthesis Bucladesine - pharmacology Clone Cells Colforsin - pharmacology Cyclosporine - pharmacology Dinoprostone - pharmacology DNA-Binding Proteins - biosynthesis DNA-Binding Proteins - physiology Enzyme Inhibitors - pharmacology Ethers, Cyclic - pharmacology Female Humans Immunosuppressive Agents - pharmacology Kinetics Lymphocyte Activation NFATC Transcription Factors Nuclear Proteins Okadaic Acid Oxazoles - pharmacology Phosphoprotein Phosphatases - antagonists & inhibitors Placenta Pregnancy Protein Phosphatase 1 Recombinant Proteins - biosynthesis Recombinant Proteins - metabolism T-Lymphocytes - drug effects T-Lymphocytes - immunology T-Lymphocytes - physiology Tacrolimus - pharmacology Tetradecanoylphorbol Acetate - pharmacology Transcription Factors - biosynthesis Transcription Factors - physiology Transfection Tumor Cells, Cultured |
| title | Regulation of the Nuclear Factor of Activated T Cells in Stably Transfected Jurkat Cell Clones |
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