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data-work-id="125785434"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/125785434/Degenerative_processes_in_the_marginal_retina_of_the_tench_Tinca_tinca_"><img alt="Research paper thumbnail of Degenerative processes in the marginal retina of the tench (Tinca tinca)" class="work-thumbnail" src="https://attachments.academia-assets.com/119765556/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/125785434/Degenerative_processes_in_the_marginal_retina_of_the_tench_Tinca_tinca_">Degenerative processes in the marginal retina of the tench (Tinca tinca)</a></div><div class="wp-workCard_item"><span>European journal of anatomy</span><span>, Aug 6, 2019</span></div><div 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href="https://www.academia.edu/125785433/Analysis_of_Kinesin_2_Function_in_Photoreceptor_Cells_Using_Synchronous_i_Cre_i_loxP_Knockout_of_i_Kif3a_i_with_i_RHO_Cre_i_"><img alt="Research paper thumbnail of Analysis of Kinesin-2 Function in Photoreceptor Cells Using Synchronous<i>Cre</i>-loxP Knockout of<i>Kif3a</i>with<i>RHO-Cre</i>" class="work-thumbnail" src="https://attachments.academia-assets.com/119765553/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/125785433/Analysis_of_Kinesin_2_Function_in_Photoreceptor_Cells_Using_Synchronous_i_Cre_i_loxP_Knockout_of_i_Kif3a_i_with_i_RHO_Cre_i_">Analysis of Kinesin-2 Function in Photoreceptor Cells Using Synchronous<i>Cre</i>-loxP Knockout of<i>Kif3a</i>with<i>RHO-Cre</i></a></div><div class="wp-workCard_item"><span>Investigative 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/></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/125785422/RasGRF2_controls_nuclear_trafficking_in_photoreceptor_cells">RasGRF2 controls nuclear trafficking in photoreceptor cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.Analyses of RasGRF1 knockout (GRF1-KO), GRF2-KO and the GRF1/2 double-KO mouse retinas, revealed specific alterations in cone photoreceptors in the GRF2-KO and GRF1/2-DKO. These alterations consist in the specific accumulation of misplaced “ectopic” nuclei in the photoreceptors segments area. The pathological displacement of cone nuclei occurred postnatally and peaked between postnatal day 11 (P11) and P15 coinciding with the so called “late migratory phase” of cone nuclei. The late migratory phase is a physiological process whereby cone nuclei move towards the outer limiting membrane (OLM) where they reach their final position. In the GRF2-KO and GRF1/2-DKO retinas this movement is deregulated and cone nuclei are located closer to the OLM and in some regions of the retina even trespass it. Using detailed inmunocytochemical analyses we have identified disruption of the OLM and accumulation of activated, phosphorylated forms of PAK, MLC2 and VASP, molecules known to participate in nuclear migration and cytoskeletal reorganization, in cone photoreceptors of GRF2-KO and GRF1/2-DKO retinas. Electroretinographic recordings show specific impairment of cone photoreceptor cells in GRF1-KO and GRF1/2-DKO retinas. These data support a critical role of GRF2 in cone nuclear migration and proper retinal development and functioning.Peer reviewe</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785422"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785422"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785422; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785422]").text(description); $(".js-view-count[data-work-id=125785422]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785422; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785422']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785422, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=125785422]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785422,"title":"RasGRF2 controls nuclear trafficking in photoreceptor cells","translated_title":"","metadata":{"abstract":"Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.Analyses of RasGRF1 knockout (GRF1-KO), GRF2-KO and the GRF1/2 double-KO mouse retinas, revealed specific alterations in cone photoreceptors in the GRF2-KO and GRF1/2-DKO. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="125785418"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/125785418/Insulin_receptor_activation_by_proinsulin_preserves_synapses_and_vision_in_retinitis_pigmentosa"><img alt="Research paper thumbnail of Insulin receptor activation by proinsulin preserves synapses and vision in retinitis pigmentosa" class="work-thumbnail" src="https://attachments.academia-assets.com/119765565/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/125785418/Insulin_receptor_activation_by_proinsulin_preserves_synapses_and_vision_in_retinitis_pigmentosa">Insulin receptor activation by proinsulin preserves synapses and vision in retinitis pigmentosa</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ABSTRACTSynaptic loss, neuronal death, and circuit remodeling are common features of central nerv...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ABSTRACTSynaptic loss, neuronal death, and circuit remodeling are common features of central nervous system neurodegenerative disorders. Retinitis pigmentosa (RP), the leading cause of inherited blindness, is a group of retinal dystrophies characterized by photoreceptor dysfunction and death. The insulin receptor, a key controller of metabolism, also regulates neuronal survival and synaptic formation, maintenance, and activity. Indeed, deficient insulin receptor signaling has been implicated in several brain neurodegenerative pathologies. We present evidence linking impaired insulin receptor signaling with RP. We describe a selective decrease in the levels of the insulin receptor and its downstream effector phospho-S6 in retinal horizontal cell axons in the rd10 mouse model of RP, as well as aberrant synapses between rod photoreceptors and the postsynaptic terminals of horizontal and bipolar cells. A gene therapy strategy to induce sustained proinsulin production restored retinal in...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="307ec268d4ac9f912337fd9d305ddfdf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119765565,"asset_id":125785418,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119765565/download_file?st=MTczMjc5MzMyMCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785418"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785418"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785418; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785418]").text(description); $(".js-view-count[data-work-id=125785418]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785418; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785418']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785418, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "307ec268d4ac9f912337fd9d305ddfdf" } } $('.js-work-strip[data-work-id=125785418]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785418,"title":"Insulin receptor activation by proinsulin preserves synapses and vision in retinitis pigmentosa","translated_title":"","metadata":{"abstract":"ABSTRACTSynaptic loss, neuronal death, and circuit remodeling are common features of central nervous system neurodegenerative disorders. Retinitis pigmentosa (RP), the leading cause of inherited blindness, is a group of retinal dystrophies characterized by photoreceptor dysfunction and death. The insulin receptor, a key controller of metabolism, also regulates neuronal survival and synaptic formation, maintenance, and activity. Indeed, deficient insulin receptor signaling has been implicated in several brain neurodegenerative pathologies. We present evidence linking impaired insulin receptor signaling with RP. We describe a selective decrease in the levels of the insulin receptor and its downstream effector phospho-S6 in retinal horizontal cell axons in the rd10 mouse model of RP, as well as aberrant synapses between rod photoreceptors and the postsynaptic terminals of horizontal and bipolar cells. 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We describe a selective decrease in the levels of the insulin receptor and its downstream effector phospho-S6 in retinal horizontal cell axons in the rd10 mouse model of RP, as well as aberrant synapses between rod photoreceptors and the postsynaptic terminals of horizontal and bipolar cells. 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Here, POS phagosomes were observed to associate with myosin-7a, and then kinesin-1, as they moved from the apical region of the RPE. Live-cell imaging showed that the phagosomes moved bidirectionally along microtubules in RPE cells, with kinesin-1 light chain 1 (KLC1) remaining associated in both directions and during pauses. Lack of KLC1 did not inhibit phagosome speed, but run length was decreased, and phagosome localization and degradation were impaired. In old mice, lack of KLC1 resulted in RPE pathogenesis that was strikingly comparable to aspects of age-related macular degeneration (AMD), with an excessive accumulation of RPE and sub-RPE deposits, as well as oxidative and inflammatory stress responses. 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These results elucidate mechanisms of POS phagosome transport in relation to degradation, and demonstrate that ...","publication_date":{"day":10,"month":1,"year":2015,"errors":{}},"publication_name":"The Journal of cell biology"},"translated_abstract":"The degradation of phagosomes, derived from the ingestion of photoreceptor outer segment (POS) disk membranes, is a major role of the retinal pigment epithelium (RPE). Here, POS phagosomes were observed to associate with myosin-7a, and then kinesin-1, as they moved from the apical region of the RPE. Live-cell imaging showed that the phagosomes moved bidirectionally along microtubules in RPE cells, with kinesin-1 light chain 1 (KLC1) remaining associated in both directions and during pauses. Lack of KLC1 did not inhibit phagosome speed, but run length was decreased, and phagosome localization and degradation were impaired. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="125785415"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/125785415/Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration"><img alt="Research paper thumbnail of Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration" class="work-thumbnail" src="https://attachments.academia-assets.com/119765574/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/125785415/Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration">Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration</a></div><div class="wp-workCard_item"><span>Proceedings of the National Academy of Sciences</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degener...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE) in the central retina. An autosomal dominant form of Stargardt macular degeneration (STGD) is caused by mutations in ELOVL4 , which is predicted to encode an enzyme involved in the elongation of long-chain fatty acids. We generated transgenic mice expressing a mutant form of human ELOVL4 that causes STGD. In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. The ELOVL4 transgenic mice thus provi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0ff0a82f6abdc8873194bf5b9bbf4036" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119765574,"asset_id":125785415,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119765574/download_file?st=MTczMjc5MzMyMCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785415"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785415"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785415; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785415]").text(description); $(".js-view-count[data-work-id=125785415]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785415; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785415']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785415, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0ff0a82f6abdc8873194bf5b9bbf4036" } } $('.js-work-strip[data-work-id=125785415]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785415,"title":"Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration","translated_title":"","metadata":{"abstract":"Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE) in the central retina. An autosomal dominant form of Stargardt macular degeneration (STGD) is caused by mutations in ELOVL4 , which is predicted to encode an enzyme involved in the elongation of long-chain fatty acids. We generated transgenic mice expressing a mutant form of human ELOVL4 that causes STGD. In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. The ELOVL4 transgenic mice thus provi...","publisher":"Proceedings of the National Academy of Sciences","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Proceedings of the National Academy of Sciences"},"translated_abstract":"Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE) in the central retina. An autosomal dominant form of Stargardt macular degeneration (STGD) is caused by mutations in ELOVL4 , which is predicted to encode an enzyme involved in the elongation of long-chain fatty acids. We generated transgenic mice expressing a mutant form of human ELOVL4 that causes STGD. In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. The ELOVL4 transgenic mice thus provi...","internal_url":"https://www.academia.edu/125785415/Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration","translated_internal_url":"","created_at":"2024-11-23T13:18:11.216-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":41262199,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":119765574,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/119765574/thumbnails/1.jpg","file_name":"ef12901688f751e37ea97ff77b19d59939aa.pdf","download_url":"https://www.academia.edu/attachments/119765574/download_file?st=MTczMjc5MzMyMCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Lipofuscin_accumulation_abnormal_electro.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/119765574/ef12901688f751e37ea97ff77b19d59939aa.pdf?1732396776=\u0026response-content-disposition=attachment%3B+filename%3DLipofuscin_accumulation_abnormal_electro.pdf\u0026Expires=1732791754\u0026Signature=RZ6wBaOvN-A7RdTSD~frDcHvHsYc6dI9UyU4rAJr-viCrjbtYLr1i-MmbtR7MmTPF2a9P8NgI7dWZA84FylyoG-Oce8rMXk~M1jmNPvq6o2pmzap3yS6bEzcxv2Av21fsZkuTx8LNU1zwdSMrz~G-yqL8B7CudXe2XpJtUizuiqy2lgyq2OWFK-nfoh10yyGv7FNItgP29mKcVHtt17V7SClMmlsR2MRaeQqiUMt3t2bYQrO~xB4dU2r~8nJJP867JnioSI2D-PaY1KxyB~rq7gkxjs8l16Em4XrHqmjpfZDE8UwEQp7hOKzLl8FKqrbZuac6FpNPt2hgo1wdWzr9g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration","translated_slug":"","page_count":6,"language":"en","content_type":"Work","owner":{"id":41262199,"first_name":"Concepcion","middle_initials":null,"last_name":"Lillo","page_name":"ConcepcionLillo","domain_name":"usal","created_at":"2016-01-11T01:04:10.047-08:00","display_name":"Concepcion 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/></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/125785422/RasGRF2_controls_nuclear_trafficking_in_photoreceptor_cells">RasGRF2 controls nuclear trafficking in photoreceptor cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.Analyses of RasGRF1 knockout (GRF1-KO), GRF2-KO and the GRF1/2 double-KO mouse retinas, revealed specific alterations in cone photoreceptors in the GRF2-KO and GRF1/2-DKO. These alterations consist in the specific accumulation of misplaced “ectopic” nuclei in the photoreceptors segments area. The pathological displacement of cone nuclei occurred postnatally and peaked between postnatal day 11 (P11) and P15 coinciding with the so called “late migratory phase” of cone nuclei. The late migratory phase is a physiological process whereby cone nuclei move towards the outer limiting membrane (OLM) where they reach their final position. In the GRF2-KO and GRF1/2-DKO retinas this movement is deregulated and cone nuclei are located closer to the OLM and in some regions of the retina even trespass it. Using detailed inmunocytochemical analyses we have identified disruption of the OLM and accumulation of activated, phosphorylated forms of PAK, MLC2 and VASP, molecules known to participate in nuclear migration and cytoskeletal reorganization, in cone photoreceptors of GRF2-KO and GRF1/2-DKO retinas. Electroretinographic recordings show specific impairment of cone photoreceptor cells in GRF1-KO and GRF1/2-DKO retinas. These data support a critical role of GRF2 in cone nuclear migration and proper retinal development and functioning.Peer reviewe</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785422"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785422"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785422; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785422]").text(description); $(".js-view-count[data-work-id=125785422]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785422; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785422']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785422, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=125785422]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785422,"title":"RasGRF2 controls nuclear trafficking in photoreceptor cells","translated_title":"","metadata":{"abstract":"Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.Analyses of RasGRF1 knockout (GRF1-KO), GRF2-KO and the GRF1/2 double-KO mouse retinas, revealed specific alterations in cone photoreceptors in the GRF2-KO and GRF1/2-DKO. 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Retinitis pigmentosa (RP), the leading cause of inherited blindness, is a group of retinal dystrophies characterized by photoreceptor dysfunction and death. The insulin receptor, a key controller of metabolism, also regulates neuronal survival and synaptic formation, maintenance, and activity. Indeed, deficient insulin receptor signaling has been implicated in several brain neurodegenerative pathologies. We present evidence linking impaired insulin receptor signaling with RP. We describe a selective decrease in the levels of the insulin receptor and its downstream effector phospho-S6 in retinal horizontal cell axons in the rd10 mouse model of RP, as well as aberrant synapses between rod photoreceptors and the postsynaptic terminals of horizontal and bipolar cells. A gene therapy strategy to induce sustained proinsulin production restored retinal in...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="307ec268d4ac9f912337fd9d305ddfdf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119765565,"asset_id":125785418,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119765565/download_file?st=MTczMjc5MzMyMCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785418"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785418"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785418; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785418]").text(description); $(".js-view-count[data-work-id=125785418]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785418; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785418']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785418, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "307ec268d4ac9f912337fd9d305ddfdf" } } $('.js-work-strip[data-work-id=125785418]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785418,"title":"Insulin receptor activation by proinsulin preserves synapses and vision in retinitis pigmentosa","translated_title":"","metadata":{"abstract":"ABSTRACTSynaptic loss, neuronal death, and circuit remodeling are common features of central nervous system neurodegenerative disorders. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="125785415"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/125785415/Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration"><img alt="Research paper thumbnail of Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration" class="work-thumbnail" src="https://attachments.academia-assets.com/119765574/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/125785415/Lipofuscin_accumulation_abnormal_electrophysiology_and_photoreceptor_degeneration_in_mutant_ELOVL4_transgenic_mice_A_model_for_macular_degeneration">Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration</a></div><div class="wp-workCard_item"><span>Proceedings of the National Academy of Sciences</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degener...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE) in the central retina. An autosomal dominant form of Stargardt macular degeneration (STGD) is caused by mutations in ELOVL4 , which is predicted to encode an enzyme involved in the elongation of long-chain fatty acids. We generated transgenic mice expressing a mutant form of human ELOVL4 that causes STGD. In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. The ELOVL4 transgenic mice thus provi...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0ff0a82f6abdc8873194bf5b9bbf4036" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":119765574,"asset_id":125785415,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/119765574/download_file?st=MTczMjc5MzMyMCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="125785415"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="125785415"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 125785415; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=125785415]").text(description); $(".js-view-count[data-work-id=125785415]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 125785415; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='125785415']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 125785415, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0ff0a82f6abdc8873194bf5b9bbf4036" } } $('.js-work-strip[data-work-id=125785415]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":125785415,"title":"Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: A model for macular degeneration","translated_title":"","metadata":{"abstract":"Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE) in the central retina. An autosomal dominant form of Stargardt macular degeneration (STGD) is caused by mutations in ELOVL4 , which is predicted to encode an enzyme involved in the elongation of long-chain fatty acids. We generated transgenic mice expressing a mutant form of human ELOVL4 that causes STGD. In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. 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In these mice, we show that accumulation by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1-(2-hyydroxyethyl)-4-[4-methyl-6-(2,6,6,-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E) is followed by RPE atrophy. Subsequently, photoreceptor degeneration occurs in the central retina in a pattern closely resembling that of human STGD and age-related macular degeneration. 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