Co-localization of the Insulin Receptor, Jun Protein and Choline Acetyltransferase in Embryonic Chick Retina
Previous work demonstrated that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) and that this increase required the AP-1 transcription factor, c-jun. Here it is...
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| Veröffentlicht in: | Experimental eye research 1998-03, Vol.66 (3), p.307-313 |
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| container_title | Experimental eye research |
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| creator | HOLDENGREBER, V. REN, Y. BEN-SHAUL, Y. HAUSMAN, R.E. |
| description | Previous work demonstrated that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) and that this increase required the AP-1 transcription factor, c-jun. Here it is shown that immediately following a 2–5 min exposure to insulin there is, in the amacrine and ganglion cells of the chick embryo retina, a transient increase in the level of jun protein followed by a long-lasting increase in ChAT. These and previous results show that insulin receptor activation is necessary for the characteristic retina developmental increase in ChAT protein and that this increase is preceded by a transient increase in the synthesis of the transcription factor c-jun in the same retina cells. The data demonstrate an intracellular signal transduction pathway from the developmentally-activated insulin receptor through c-jun to ChAT and cholinergic differentiation. |
| doi_str_mv | 10.1006/exer.1997.0431 |
| format | Article |
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Here it is shown that immediately following a 2–5 min exposure to insulin there is, in the amacrine and ganglion cells of the chick embryo retina, a transient increase in the level of jun protein followed by a long-lasting increase in ChAT. These and previous results show that insulin receptor activation is necessary for the characteristic retina developmental increase in ChAT protein and that this increase is preceded by a transient increase in the synthesis of the transcription factor c-jun in the same retina cells. The data demonstrate an intracellular signal transduction pathway from the developmentally-activated insulin receptor through c-jun to ChAT and cholinergic differentiation.</description><identifier>ISSN: 0014-4835</identifier><identifier>EISSN: 1096-0007</identifier><identifier>DOI: 10.1006/exer.1997.0431</identifier><identifier>PMID: 9533858</identifier><identifier>CODEN: EXERA6</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Cell Differentiation ; ChAT ; Chick Embryo ; Choline O-Acetyltransferase - metabolism ; Embryology: invertebrates and vertebrates. Teratology ; Fundamental and applied biological sciences. Psychology ; Immunohistochemistry ; insulin ; Insulin - pharmacology ; jun ; Molecular embryology ; neurogenesis ; Proto-Oncogene Proteins c-jun - metabolism ; Receptor, Insulin - metabolism ; Retina - embryology ; Retina - metabolism ; retina development ; Retinal Ganglion Cells - metabolism</subject><ispartof>Experimental eye research, 1998-03, Vol.66 (3), p.307-313</ispartof><rights>1998 Academic Press</rights><rights>1998 INIST-CNRS</rights><rights>Copyright 1998 Academic Press Limited.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-abae5ca195f8652de2e3f6d4222439840c2abf6f493d18f7ce30dfa03c7e0403</citedby><cites>FETCH-LOGICAL-c408t-abae5ca195f8652de2e3f6d4222439840c2abf6f493d18f7ce30dfa03c7e0403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/exer.1997.0431$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2228873$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9533858$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HOLDENGREBER, V.</creatorcontrib><creatorcontrib>REN, Y.</creatorcontrib><creatorcontrib>BEN-SHAUL, Y.</creatorcontrib><creatorcontrib>HAUSMAN, R.E.</creatorcontrib><title>Co-localization of the Insulin Receptor, Jun Protein and Choline Acetyltransferase in Embryonic Chick Retina</title><title>Experimental eye research</title><addtitle>Exp Eye Res</addtitle><description>Previous work demonstrated that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) and that this increase required the AP-1 transcription factor, c-jun. Here it is shown that immediately following a 2–5 min exposure to insulin there is, in the amacrine and ganglion cells of the chick embryo retina, a transient increase in the level of jun protein followed by a long-lasting increase in ChAT. These and previous results show that insulin receptor activation is necessary for the characteristic retina developmental increase in ChAT protein and that this increase is preceded by a transient increase in the synthesis of the transcription factor c-jun in the same retina cells. The data demonstrate an intracellular signal transduction pathway from the developmentally-activated insulin receptor through c-jun to ChAT and cholinergic differentiation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Differentiation</subject><subject>ChAT</subject><subject>Chick Embryo</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunohistochemistry</subject><subject>insulin</subject><subject>Insulin - pharmacology</subject><subject>jun</subject><subject>Molecular embryology</subject><subject>neurogenesis</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Receptor, Insulin - metabolism</subject><subject>Retina - embryology</subject><subject>Retina - metabolism</subject><subject>retina development</subject><subject>Retinal Ganglion Cells - metabolism</subject><issn>0014-4835</issn><issn>1096-0007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFvGyEQRlHVKnXSXnuLxKHqqesMC7sLx8hym1SRWlW5I8wOCs0aXGCjuL8-WLZy62mkmcc3wyPkE4MlA-iv8BnTkik1LEFw9oYsGKi-AYDhLVkAMNEIybv35DznP7XLxSDOyJnqOJedXJBpFZspWjP5f6b4GGh0tDwgvQ15nnygv9HirsT0lf6YA_2VYsHaNWGkq4dYAaTXFst-KsmE7DCZjLQC6-0m7WPwtmLePtaY4oP5QN45M2X8eKoX5P7b-n5109z9_H67ur5rrABZGrMx2FnDVOdk37UjtshdP4q2bQVXUoBtzcb1Tig-MukGixxGZ4DbAUEAvyBfjrG7FP_OmIve-mxxmkzAOGc9KMXblskKLo-gTTHnhE7vkt-atNcM9MGuPtjVB7v6YLc-uDwlz5stjq_4SWedfz7NTa5OXZVifX7F6gekHHjF5BHDKuHJ1xXZegwWR5_QFj1G_78LXgAv_5b4</recordid><startdate>19980301</startdate><enddate>19980301</enddate><creator>HOLDENGREBER, V.</creator><creator>REN, Y.</creator><creator>BEN-SHAUL, Y.</creator><creator>HAUSMAN, R.E.</creator><general>Elsevier Ltd</general><general>Elsevier</general><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>7X8</scope></search><sort><creationdate>19980301</creationdate><title>Co-localization of the Insulin Receptor, Jun Protein and Choline Acetyltransferase in Embryonic Chick Retina</title><author>HOLDENGREBER, V. ; REN, Y. ; BEN-SHAUL, Y. ; HAUSMAN, R.E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-abae5ca195f8652de2e3f6d4222439840c2abf6f493d18f7ce30dfa03c7e0403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Differentiation</topic><topic>ChAT</topic><topic>Chick Embryo</topic><topic>Choline O-Acetyltransferase - metabolism</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunohistochemistry</topic><topic>insulin</topic><topic>Insulin - pharmacology</topic><topic>jun</topic><topic>Molecular embryology</topic><topic>neurogenesis</topic><topic>Proto-Oncogene Proteins c-jun - metabolism</topic><topic>Receptor, Insulin - metabolism</topic><topic>Retina - embryology</topic><topic>Retina - metabolism</topic><topic>retina development</topic><topic>Retinal Ganglion Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HOLDENGREBER, V.</creatorcontrib><creatorcontrib>REN, Y.</creatorcontrib><creatorcontrib>BEN-SHAUL, Y.</creatorcontrib><creatorcontrib>HAUSMAN, R.E.</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Experimental eye research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HOLDENGREBER, V.</au><au>REN, Y.</au><au>BEN-SHAUL, Y.</au><au>HAUSMAN, R.E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Co-localization of the Insulin Receptor, Jun Protein and Choline Acetyltransferase in Embryonic Chick Retina</atitle><jtitle>Experimental eye research</jtitle><addtitle>Exp Eye Res</addtitle><date>1998-03-01</date><risdate>1998</risdate><volume>66</volume><issue>3</issue><spage>307</spage><epage>313</epage><pages>307-313</pages><issn>0014-4835</issn><eissn>1096-0007</eissn><coden>EXERA6</coden><abstract>Previous work demonstrated that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) and that this increase required the AP-1 transcription factor, c-jun. 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| ispartof | Experimental eye research, 1998-03, Vol.66 (3), p.307-313 |
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| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Biological and medical sciences Blotting, Western Cell Differentiation ChAT Chick Embryo Choline O-Acetyltransferase - metabolism Embryology: invertebrates and vertebrates. Teratology Fundamental and applied biological sciences. Psychology Immunohistochemistry insulin Insulin - pharmacology jun Molecular embryology neurogenesis Proto-Oncogene Proteins c-jun - metabolism Receptor, Insulin - metabolism Retina - embryology Retina - metabolism retina development Retinal Ganglion Cells - metabolism |
| title | Co-localization of the Insulin Receptor, Jun Protein and Choline Acetyltransferase in Embryonic Chick Retina |
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