A Disintegrin and Metalloproteinase10 (ADAM10) Regulates NOTCH Signaling during Early Retinal Development
ADAM10 and ADAM17 are two closely related members of the ADAM (a disintegrin and metalloprotease) family of membrane-bound sheddases, which proteolytically cleave surface membrane proteins. Both ADAM10 and ADAM17 have been implicated in the proteolytic cleavage of NOTCH receptors and as such regulat...
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| description | ADAM10 and ADAM17 are two closely related members of the ADAM (a disintegrin and metalloprotease) family of membrane-bound sheddases, which proteolytically cleave surface membrane proteins. Both ADAM10 and ADAM17 have been implicated in the proteolytic cleavage of NOTCH receptors and as such regulators of NOTCH signaling. During retinal development, NOTCH signaling facilitates retinal neurogenesis by maintaining progenitor cells in a proliferative state and by mediating retinal cell fates. However, the roles of ADAM10 and ADAM17 in the retina are not well defined. In this study, we set out to clarify the roles of ADAM10 and ADAM17 during early retinal development. The retinal phenotype of conditionally abated Adam17 retinae (Adam17 CKO) did not differ from the controls whereas conditionally ablated Adam10 retinae (Adam10 CKO) exhibited abnormal morphogenesis characterized by the formation of rosettes and a loss of retinal laminae phenotypically similar to morphological abnormalities identified in mice with retinal NOTCH signaling deficiency. Additionally, Adam10 CKO retinae exhibited abnormal neurogenesis characterized by fewer proliferating progenitor cells and greater differentiation of early photoreceptors and retinal ganglion cells. Moreover, constitutive activation of the NOTCH1-intracellular domain (N1-ICD) rescued Adam10 CKO abnormal neurogenesis, as well as abnormal retinal morphology by maintaining retinal cells in the progenitor state. Collectively these findings provide in vivo genetic evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling. |
| doi_str_mv | 10.1371/journal.pone.0156184 |
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Both ADAM10 and ADAM17 have been implicated in the proteolytic cleavage of NOTCH receptors and as such regulators of NOTCH signaling. During retinal development, NOTCH signaling facilitates retinal neurogenesis by maintaining progenitor cells in a proliferative state and by mediating retinal cell fates. However, the roles of ADAM10 and ADAM17 in the retina are not well defined. In this study, we set out to clarify the roles of ADAM10 and ADAM17 during early retinal development. The retinal phenotype of conditionally abated Adam17 retinae (Adam17 CKO) did not differ from the controls whereas conditionally ablated Adam10 retinae (Adam10 CKO) exhibited abnormal morphogenesis characterized by the formation of rosettes and a loss of retinal laminae phenotypically similar to morphological abnormalities identified in mice with retinal NOTCH signaling deficiency. Additionally, Adam10 CKO retinae exhibited abnormal neurogenesis characterized by fewer proliferating progenitor cells and greater differentiation of early photoreceptors and retinal ganglion cells. Moreover, constitutive activation of the NOTCH1-intracellular domain (N1-ICD) rescued Adam10 CKO abnormal neurogenesis, as well as abnormal retinal morphology by maintaining retinal cells in the progenitor state. Collectively these findings provide in vivo genetic evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0156184</identifier><identifier>PMID: 27224017</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; ADAM10 Protein - genetics ; ADAM10 Protein - metabolism ; ADAM17 Protein - genetics ; ADAM17 Protein - metabolism ; Amyloid Precursor Protein Secretases - genetics ; Amyloid Precursor Protein Secretases - metabolism ; Animals ; Biology and Life Sciences ; Cell adhesion & migration ; Cell Differentiation ; Cell Proliferation ; Cells (biology) ; Cellular biology ; Cellular signal transduction ; Developmental biology ; Genetic aspects ; Laminates ; Ligands ; Medicine and Health Sciences ; Membrane proteins ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Metalloenzymes ; Metalloproteinase ; Mice ; Morphogenesis ; Neurobiology ; Neurogenesis ; Neurosciences ; Notch protein ; Notch1 protein ; Phenotypes ; Photoreceptors ; Physiological aspects ; Progenitor cells ; Proteins ; Proteolysis ; Receptors ; Receptors, Notch - metabolism ; Regulators ; Research and Analysis Methods ; Retina ; Retina - cytology ; Retina - growth & development ; Retina - metabolism ; Retinal cells ; Retinal ganglion cells ; Signal Transduction ; Signaling ; Social Sciences ; Stem cells</subject><ispartof>PloS one, 2016-05, Vol.11 (5), p.e0156184-e0156184</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Toonen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Toonen et al 2016 Toonen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-b5bf4f30b3e44bbe85184703556e7037695e0d8c68a3ad4323121bb91e34d4d93</citedby><cites>FETCH-LOGICAL-c692t-b5bf4f30b3e44bbe85184703556e7037695e0d8c68a3ad4323121bb91e34d4d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880208/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880208/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27224017$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kihara, Alexandre Hiroaki</contributor><creatorcontrib>Toonen, Joseph A</creatorcontrib><creatorcontrib>Ronchetti, Adam</creatorcontrib><creatorcontrib>Sidjanin, D J</creatorcontrib><title>A Disintegrin and Metalloproteinase10 (ADAM10) Regulates NOTCH Signaling during Early Retinal Development</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>ADAM10 and ADAM17 are two closely related members of the ADAM (a disintegrin and metalloprotease) family of membrane-bound sheddases, which proteolytically cleave surface membrane proteins. Both ADAM10 and ADAM17 have been implicated in the proteolytic cleavage of NOTCH receptors and as such regulators of NOTCH signaling. During retinal development, NOTCH signaling facilitates retinal neurogenesis by maintaining progenitor cells in a proliferative state and by mediating retinal cell fates. However, the roles of ADAM10 and ADAM17 in the retina are not well defined. In this study, we set out to clarify the roles of ADAM10 and ADAM17 during early retinal development. The retinal phenotype of conditionally abated Adam17 retinae (Adam17 CKO) did not differ from the controls whereas conditionally ablated Adam10 retinae (Adam10 CKO) exhibited abnormal morphogenesis characterized by the formation of rosettes and a loss of retinal laminae phenotypically similar to morphological abnormalities identified in mice with retinal NOTCH signaling deficiency. Additionally, Adam10 CKO retinae exhibited abnormal neurogenesis characterized by fewer proliferating progenitor cells and greater differentiation of early photoreceptors and retinal ganglion cells. Moreover, constitutive activation of the NOTCH1-intracellular domain (N1-ICD) rescued Adam10 CKO abnormal neurogenesis, as well as abnormal retinal morphology by maintaining retinal cells in the progenitor state. Collectively these findings provide in vivo genetic evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.</description><subject>Abnormalities</subject><subject>ADAM10 Protein - genetics</subject><subject>ADAM10 Protein - metabolism</subject><subject>ADAM17 Protein - genetics</subject><subject>ADAM17 Protein - metabolism</subject><subject>Amyloid Precursor Protein Secretases - genetics</subject><subject>Amyloid Precursor Protein Secretases - metabolism</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Cell adhesion & migration</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Cells (biology)</subject><subject>Cellular biology</subject><subject>Cellular signal transduction</subject><subject>Developmental biology</subject><subject>Genetic aspects</subject><subject>Laminates</subject><subject>Ligands</subject><subject>Medicine and Health Sciences</subject><subject>Membrane proteins</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Metalloenzymes</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Morphogenesis</subject><subject>Neurobiology</subject><subject>Neurogenesis</subject><subject>Neurosciences</subject><subject>Notch protein</subject><subject>Notch1 protein</subject><subject>Phenotypes</subject><subject>Photoreceptors</subject><subject>Physiological aspects</subject><subject>Progenitor cells</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>Receptors</subject><subject>Receptors, Notch - metabolism</subject><subject>Regulators</subject><subject>Research and Analysis Methods</subject><subject>Retina</subject><subject>Retina - cytology</subject><subject>Retina - growth & development</subject><subject>Retina - metabolism</subject><subject>Retinal cells</subject><subject>Retinal ganglion cells</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Social Sciences</subject><subject>Stem cells</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</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><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkLbRYs_E-cGqVoHVNqotAG3lpOcpK7cuNjOxP497ppNDdoFysWJ7Od9fc6xT5K8xWiKaY4_rW3vOmWmW9vBFGGeYcGeJce4oGSSEUSfH_wfJa-8XyPEqciyl8kRyQlhCOfHiZ6lc-11F6B1uktVV6dXEJQxdutsAN0pDxilp7P57Aqjs_Qa2t6oAD79vvxx_i290W1MQndtWvduFy6UM3cRC1Fq0jncQrTaQBdeJy8aZTy8GeJJ8vPLRbSYXC6_Ls5nl5MqK0iYlLxsWENRSYGxsgTBY105opxnEEOeFRxQLapMKKpqRgnFBJdlgYGymtUFPUne7323xno5dMlLnBeYEoEEicRiT9RWreXW6Y1yd9IqLe8XrGulckFXBqSoYlYMCOMlMJHFrHidYYWaklU1z3n0-jyc1pcbqKtYqFNmZDre6fRKtvZWMiEQQSIanA4Gzv7uwQe50b4CY1QHtr_Pm1CBCrJDP_yDPl3dQLUqFqC7xsZzq52pnDFOKS9ymkVq-gQVvxo2uopPqtFxfSQ4GwkiE-BPaFXvvVzcXP8_u_w1Zj8esCtQJqy8NX3QtvNjkO3BylnvHTSPTcZI7ibioRtyNxFymIgoe3d4QY-ihxGgfwFNZAOz</recordid><startdate>20160525</startdate><enddate>20160525</enddate><creator>Toonen, Joseph A</creator><creator>Ronchetti, Adam</creator><creator>Sidjanin, D J</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160525</creationdate><title>A Disintegrin and Metalloproteinase10 (ADAM10) Regulates NOTCH Signaling during Early Retinal Development</title><author>Toonen, Joseph A ; Ronchetti, Adam ; Sidjanin, D J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-b5bf4f30b3e44bbe85184703556e7037695e0d8c68a3ad4323121bb91e34d4d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Abnormalities</topic><topic>ADAM10 Protein - genetics</topic><topic>ADAM10 Protein - metabolism</topic><topic>ADAM17 Protein - genetics</topic><topic>ADAM17 Protein - metabolism</topic><topic>Amyloid Precursor Protein Secretases - genetics</topic><topic>Amyloid Precursor Protein Secretases - metabolism</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Cell adhesion & migration</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>Cells (biology)</topic><topic>Cellular biology</topic><topic>Cellular signal transduction</topic><topic>Developmental biology</topic><topic>Genetic aspects</topic><topic>Laminates</topic><topic>Ligands</topic><topic>Medicine and Health Sciences</topic><topic>Membrane proteins</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Metalloenzymes</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Morphogenesis</topic><topic>Neurobiology</topic><topic>Neurogenesis</topic><topic>Neurosciences</topic><topic>Notch protein</topic><topic>Notch1 protein</topic><topic>Phenotypes</topic><topic>Photoreceptors</topic><topic>Physiological aspects</topic><topic>Progenitor cells</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>Receptors</topic><topic>Receptors, Notch - metabolism</topic><topic>Regulators</topic><topic>Research and Analysis Methods</topic><topic>Retina</topic><topic>Retina - cytology</topic><topic>Retina - growth & development</topic><topic>Retina - metabolism</topic><topic>Retinal cells</topic><topic>Retinal ganglion cells</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Social Sciences</topic><topic>Stem cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toonen, Joseph A</creatorcontrib><creatorcontrib>Ronchetti, Adam</creatorcontrib><creatorcontrib>Sidjanin, D J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toonen, Joseph A</au><au>Ronchetti, Adam</au><au>Sidjanin, D J</au><au>Kihara, Alexandre Hiroaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Disintegrin and Metalloproteinase10 (ADAM10) Regulates NOTCH Signaling during Early Retinal Development</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-05-25</date><risdate>2016</risdate><volume>11</volume><issue>5</issue><spage>e0156184</spage><epage>e0156184</epage><pages>e0156184-e0156184</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>ADAM10 and ADAM17 are two closely related members of the ADAM (a disintegrin and metalloprotease) family of membrane-bound sheddases, which proteolytically cleave surface membrane proteins. Both ADAM10 and ADAM17 have been implicated in the proteolytic cleavage of NOTCH receptors and as such regulators of NOTCH signaling. During retinal development, NOTCH signaling facilitates retinal neurogenesis by maintaining progenitor cells in a proliferative state and by mediating retinal cell fates. However, the roles of ADAM10 and ADAM17 in the retina are not well defined. In this study, we set out to clarify the roles of ADAM10 and ADAM17 during early retinal development. The retinal phenotype of conditionally abated Adam17 retinae (Adam17 CKO) did not differ from the controls whereas conditionally ablated Adam10 retinae (Adam10 CKO) exhibited abnormal morphogenesis characterized by the formation of rosettes and a loss of retinal laminae phenotypically similar to morphological abnormalities identified in mice with retinal NOTCH signaling deficiency. Additionally, Adam10 CKO retinae exhibited abnormal neurogenesis characterized by fewer proliferating progenitor cells and greater differentiation of early photoreceptors and retinal ganglion cells. Moreover, constitutive activation of the NOTCH1-intracellular domain (N1-ICD) rescued Adam10 CKO abnormal neurogenesis, as well as abnormal retinal morphology by maintaining retinal cells in the progenitor state. Collectively these findings provide in vivo genetic evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27224017</pmid><doi>10.1371/journal.pone.0156184</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Abnormalities ADAM10 Protein - genetics ADAM10 Protein - metabolism ADAM17 Protein - genetics ADAM17 Protein - metabolism Amyloid Precursor Protein Secretases - genetics Amyloid Precursor Protein Secretases - metabolism Animals Biology and Life Sciences Cell adhesion & migration Cell Differentiation Cell Proliferation Cells (biology) Cellular biology Cellular signal transduction Developmental biology Genetic aspects Laminates Ligands Medicine and Health Sciences Membrane proteins Membrane Proteins - genetics Membrane Proteins - metabolism Metalloenzymes Metalloproteinase Mice Morphogenesis Neurobiology Neurogenesis Neurosciences Notch protein Notch1 protein Phenotypes Photoreceptors Physiological aspects Progenitor cells Proteins Proteolysis Receptors Receptors, Notch - metabolism Regulators Research and Analysis Methods Retina Retina - cytology Retina - growth & development Retina - metabolism Retinal cells Retinal ganglion cells Signal Transduction Signaling Social Sciences Stem cells |
| title | A Disintegrin and Metalloproteinase10 (ADAM10) Regulates NOTCH Signaling during Early Retinal Development |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T13%3A13%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20Disintegrin%20and%20Metalloproteinase10%20(ADAM10)%20Regulates%20NOTCH%20Signaling%20during%20Early%20Retinal%20Development&rft.jtitle=PloS%20one&rft.au=Toonen,%20Joseph%20A&rft.date=2016-05-25&rft.volume=11&rft.issue=5&rft.spage=e0156184&rft.epage=e0156184&rft.pages=e0156184-e0156184&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0156184&rft_dat=%3Cgale_plos_%3EA453359736%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1791328082&rft_id=info:pmid/27224017&rft_galeid=A453359736&rft_doaj_id=oai_doaj_org_article_8cc694e245be4860b35d61a0fb4cd575&rfr_iscdi=true |