Insulin response of a hybrid amylase/CAT gene in transgenic mice
Expression of an amylase/CAT hybrid gene was analyzed in transgenic mice. The amylase promoter was derived from a pancreatic amylase gene whose expression is repressed in diabetic animals. Pancreas-specific expression of the amylase/chloramphenicol acetyl-transferase (CAT) construct was observed in...
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| Veröffentlicht in: | The Journal of biological chemistry 1988-11, Vol.263 (32), p.16519-16522 |
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| container_issue | 32 |
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| container_title | The Journal of biological chemistry |
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| creator | Osborn, L Rosenberg, M P Keller, S A Ting, C N Meisler, M H |
| description | Expression of an amylase/CAT hybrid gene was analyzed in transgenic mice. The amylase promoter was derived from a pancreatic amylase gene whose expression is repressed in diabetic animals. Pancreas-specific expression of the amylase/chloramphenicol acetyl-transferase (CAT) construct was observed in two independent transgenic lines. Correct initiation of transcription was demonstrated by protection of an anti-sense riboprobe. To evaluate the insulin dependence of the hybrid gene, diabetes was induced by treatment with streptozotocin. As a result of this treatment, pancreatic CAT activity was reduced to undetectable levels. Subsequent administration of insulin restored CAT activity to normal levels. The abundance of CAT transcripts was also greatly reduced in diabetic pancreas. These studies localize the determinants of pancreas specificity and insulin dependence to the region between -208 and +19 of the mouse pancreatic Amy-2.2 gene. The results are consistent with an effect of insulin on amylase transcription, rather than post-transcriptional regulation of mRNA processing or stability. |
| doi_str_mv | 10.1016/S0021-9258(18)37419-2 |
| format | Article |
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The amylase promoter was derived from a pancreatic amylase gene whose expression is repressed in diabetic animals. Pancreas-specific expression of the amylase/chloramphenicol acetyl-transferase (CAT) construct was observed in two independent transgenic lines. Correct initiation of transcription was demonstrated by protection of an anti-sense riboprobe. To evaluate the insulin dependence of the hybrid gene, diabetes was induced by treatment with streptozotocin. As a result of this treatment, pancreatic CAT activity was reduced to undetectable levels. Subsequent administration of insulin restored CAT activity to normal levels. The abundance of CAT transcripts was also greatly reduced in diabetic pancreas. These studies localize the determinants of pancreas specificity and insulin dependence to the region between -208 and +19 of the mouse pancreatic Amy-2.2 gene. The results are consistent with an effect of insulin on amylase transcription, rather than post-transcriptional regulation of mRNA processing or stability.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/S0021-9258(18)37419-2</identifier><identifier>PMID: 2460451</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Amylases - genetics ; Animals ; Base Sequence ; Biological and medical sciences ; Biotechnology ; Cell Line ; Chloramphenicol O-Acetyltransferase - genetics ; Diabetes Mellitus, Experimental - genetics ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Genetic engineering ; Genetic technics ; Insulin - metabolism ; Methods. Procedures. Technologies ; Mice ; Mice, Transgenic ; Molecular and cellular biology ; Molecular genetics ; Molecular Sequence Data ; Nucleotide Mapping ; Pancreas - enzymology ; Promoter Regions, Genetic ; Transcription, Genetic ; Vectors (cloning, transfer, expression). Insertion sequences and transposons</subject><ispartof>The Journal of biological chemistry, 1988-11, Vol.263 (32), p.16519-16522</ispartof><rights>1988 © 1988 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-9a45498d0f5f297ada277d626c13b936d3b8462f705f0374f323acd485a048b23</citedby><cites>FETCH-LOGICAL-c496t-9a45498d0f5f297ada277d626c13b936d3b8462f705f0374f323acd485a048b23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7169747$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2460451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Osborn, L</creatorcontrib><creatorcontrib>Rosenberg, M P</creatorcontrib><creatorcontrib>Keller, S A</creatorcontrib><creatorcontrib>Ting, C N</creatorcontrib><creatorcontrib>Meisler, M H</creatorcontrib><title>Insulin response of a hybrid amylase/CAT gene in transgenic mice</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Expression of an amylase/CAT hybrid gene was analyzed in transgenic mice. The amylase promoter was derived from a pancreatic amylase gene whose expression is repressed in diabetic animals. Pancreas-specific expression of the amylase/chloramphenicol acetyl-transferase (CAT) construct was observed in two independent transgenic lines. Correct initiation of transcription was demonstrated by protection of an anti-sense riboprobe. To evaluate the insulin dependence of the hybrid gene, diabetes was induced by treatment with streptozotocin. As a result of this treatment, pancreatic CAT activity was reduced to undetectable levels. Subsequent administration of insulin restored CAT activity to normal levels. The abundance of CAT transcripts was also greatly reduced in diabetic pancreas. These studies localize the determinants of pancreas specificity and insulin dependence to the region between -208 and +19 of the mouse pancreatic Amy-2.2 gene. The results are consistent with an effect of insulin on amylase transcription, rather than post-transcriptional regulation of mRNA processing or stability.</description><subject>Amylases - genetics</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Cell Line</subject><subject>Chloramphenicol O-Acetyltransferase - genetics</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Genetic engineering</subject><subject>Genetic technics</subject><subject>Insulin - metabolism</subject><subject>Methods. Procedures. Technologies</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Molecular Sequence Data</subject><subject>Nucleotide Mapping</subject><subject>Pancreas - enzymology</subject><subject>Promoter Regions, Genetic</subject><subject>Transcription, Genetic</subject><subject>Vectors (cloning, transfer, expression). Insertion sequences and transposons</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtvUzEQRi0EKiHwEyrdBUKwuNTj5_UKqohHpUosKBI7y9ceN0b3EewElH-P00RhWW9G1pwZfz6EXAJ9DxTU1XdKGbSGye4tdO-4FmBa9oQsgHa85RJ-PiWLM_KcvCjlF61HGLggF0woKiQsyMebqeyGNDUZy2aeCjZzbFyz3vc5hcaN-8EVvFpd3zX3OGFTwW12U6mX5JsxeXxJnkU3FHx1qkvy4_Onu9XX9vbbl5vV9W3rhVHb1jghhekCjTIyo11wTOugmPLAe8NV4H0nFIuaykjrZyJn3PkgOumo6HrGl-TNce8mz793WLZ2TMXjMLgJ512xuhNGGiEfBUGC4cZABeUR9HkuJWO0m5xGl_cWqD0otg-K7cGfhc4-KLaHJJenB3b9iOE8dXJa-69PfVe8G2L15VM5YxqU0UL_x9bpfv03ZbR9mv0aR8sUt5xZUIekS_LhiGGV-ydhtsUnnDyGOuK3Nszpkbz_ABaAoUc</recordid><startdate>19881115</startdate><enddate>19881115</enddate><creator>Osborn, L</creator><creator>Rosenberg, M P</creator><creator>Keller, S A</creator><creator>Ting, C N</creator><creator>Meisler, M H</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19881115</creationdate><title>Insulin response of a hybrid amylase/CAT gene in transgenic mice</title><author>Osborn, L ; Rosenberg, M P ; Keller, S A ; Ting, C N ; Meisler, M H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-9a45498d0f5f297ada277d626c13b936d3b8462f705f0374f323acd485a048b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Amylases - genetics</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Cell Line</topic><topic>Chloramphenicol O-Acetyltransferase - genetics</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Genetic engineering</topic><topic>Genetic technics</topic><topic>Insulin - metabolism</topic><topic>Methods. Procedures. Technologies</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Molecular Sequence Data</topic><topic>Nucleotide Mapping</topic><topic>Pancreas - enzymology</topic><topic>Promoter Regions, Genetic</topic><topic>Transcription, Genetic</topic><topic>Vectors (cloning, transfer, expression). Insertion sequences and transposons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Osborn, L</creatorcontrib><creatorcontrib>Rosenberg, M P</creatorcontrib><creatorcontrib>Keller, S A</creatorcontrib><creatorcontrib>Ting, C N</creatorcontrib><creatorcontrib>Meisler, M H</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Osborn, L</au><au>Rosenberg, M P</au><au>Keller, S A</au><au>Ting, C N</au><au>Meisler, M H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin response of a hybrid amylase/CAT gene in transgenic mice</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1988-11-15</date><risdate>1988</risdate><volume>263</volume><issue>32</issue><spage>16519</spage><epage>16522</epage><pages>16519-16522</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>Expression of an amylase/CAT hybrid gene was analyzed in transgenic mice. The amylase promoter was derived from a pancreatic amylase gene whose expression is repressed in diabetic animals. Pancreas-specific expression of the amylase/chloramphenicol acetyl-transferase (CAT) construct was observed in two independent transgenic lines. Correct initiation of transcription was demonstrated by protection of an anti-sense riboprobe. To evaluate the insulin dependence of the hybrid gene, diabetes was induced by treatment with streptozotocin. As a result of this treatment, pancreatic CAT activity was reduced to undetectable levels. Subsequent administration of insulin restored CAT activity to normal levels. The abundance of CAT transcripts was also greatly reduced in diabetic pancreas. These studies localize the determinants of pancreas specificity and insulin dependence to the region between -208 and +19 of the mouse pancreatic Amy-2.2 gene. The results are consistent with an effect of insulin on amylase transcription, rather than post-transcriptional regulation of mRNA processing or stability.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>2460451</pmid><doi>10.1016/S0021-9258(18)37419-2</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Amylases - genetics Animals Base Sequence Biological and medical sciences Biotechnology Cell Line Chloramphenicol O-Acetyltransferase - genetics Diabetes Mellitus, Experimental - genetics Fundamental and applied biological sciences. Psychology Gene expression Genetic engineering Genetic technics Insulin - metabolism Methods. Procedures. Technologies Mice Mice, Transgenic Molecular and cellular biology Molecular genetics Molecular Sequence Data Nucleotide Mapping Pancreas - enzymology Promoter Regions, Genetic Transcription, Genetic Vectors (cloning, transfer, expression). Insertion sequences and transposons |
| title | Insulin response of a hybrid amylase/CAT gene in transgenic mice |
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