{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:49981"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:49981","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Subzelluläre Lokalisation des Y-box-Proteins-1 (YB-1) in Mesangialzellen und Charakterisierung der dafür verantwortlichen Proteindomänen","abstract":"As a DNA- and RNA binding protein the cold-shock protein YB-1 serves multiple functions in the nucleus and cytoplasm, e.g. regulating transcription, RNA-processing, -translation and –storage. In the present study we examined the expression and localisation pattern of YB-1 in various models of glomerular diseases. Furthermore we determined protein regions involved in the regulation of YB-1 localisation. In glomeruli of healthy rat kidneys YB-1 is detected exclusively in the nucleus by means of immunohistochemistry with two different antibodies against YB-1. In the course of the Ant-Thy 1.1- nephritis YB-1 changes its localisation and expression pattern. Within one day YB-1 localizes to the perinuclear region of cells within all glomeruli . In the course of the disease the strongest cytoplasmic YB-1 signal coincided with the peak mesangial cell activation/proliferation between days 4 and 6 and was detected in a mesangial distribution pattern. With resolution of the disease at day 31 with complete morphological restitution was associated with YB-1 relocalisation to the nucleus. In the course of different other models of rat glomerular disease YB-1 remained nuclear. In the second part of the study we examined YB-1 localisation in the in vitro model of proliferating rat mesangial cells, which are activated in cell culture conditions. In these cells endogenous YB-1 as well as transfected GFP-YB-1-proteins was detected in the cytoplasm. Using cell cycle inhibitors we tried to arrest the rat mesangial cells. Only after treatment with roscovitine, a specific CDK- inhibitor, YB-1 translocated into the nucleus. Cloning various deletion construct of YB-1 with a fluorescent tag we identified three nuclear localisation signals (NLS: AS 185-194, AS 149-156, AS 276-292) and two cytoplasmic localisation signals or nuclear export signals ( ZLS: AS 1-57, AS 52-146). Experiments using leptomycin B as an inhibitor of the CRM1 dependent nuclear export could reveal a CRM-1 independent export of YB-1. In summary these results document an increased expression and translocation of YB-1 in mesangial cells in the course of glomerulonephritis, therefore YB-1 has pivotal role coordinating inflammatory processes in glomerular disease.","abstract_html":"As a DNA- and RNA binding protein the cold-shock protein YB-1 serves multiple functions in the nucleus and cytoplasm, e.g. regulating transcription, RNA-processing, -translation and –storage. In the present study we examined the expression and localisation pattern of YB-1 in various models of glomerular diseases. Furthermore we determined protein regions involved in the regulation of YB-1 localisation. In glomeruli of healthy rat kidneys YB-1 is detected exclusively in the nucleus by means of immunohistochemistry with two different antibodies against YB-1. In the course of the Ant-Thy 1.1- nephritis YB-1 changes its localisation and expression pattern. Within one day YB-1 localizes to the perinuclear region of cells within all glomeruli . In the course of the disease the strongest cytoplasmic YB-1 signal coincided with the peak mesangial cell activation/proliferation between days 4 and 6 and was detected in a mesangial distribution pattern. With resolution of the disease at day 31 with complete morphological restitution was associated with YB-1 relocalisation to the nucleus. In the course of different other models of rat glomerular disease YB-1 remained nuclear. In the second part of the study we examined YB-1 localisation in the in vitro model of proliferating rat mesangial cells, which are activated in cell culture conditions. In these cells endogenous YB-1 as well as transfected GFP-YB-1-proteins was detected in the cytoplasm. Using cell cycle inhibitors we tried to arrest the rat mesangial cells. Only after treatment with roscovitine, a specific CDK- inhibitor, YB-1 translocated into the nucleus. Cloning various deletion construct of YB-1 with a fluorescent tag we identified three nuclear localisation signals (NLS: AS 185-194, AS 149-156, AS 276-292) and two cytoplasmic localisation signals or nuclear export signals ( ZLS: AS 1-57, AS 52-146). Experiments using leptomycin B as an inhibitor of the CRM1 dependent nuclear export could reveal a CRM-1 independent export of YB-1. In summary these results document an increased expression and translocation of YB-1 in mesangial cells in the course of glomerulonephritis, therefore YB-1 has pivotal role coordinating inflammatory processes in glomerular disease.","abstract_has_math":false,"creators":["Martinkus, Sandra"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Mertens, Peter René"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008","date_published":"2008","updated_at":"2026-07-30T19:40:16Z","subjects":["info:eu-repo/classification/ddc/610","Glomerulonephritis","Mesangiale Immunglobulin-A-Glomerulonephritis","Zellzyklus","Grün fluoreszierendes Protein","Transkriptionsfaktor","Medizin","YB-1","NLS","NES","Roscovitin","Leptomycin B","roscovitine"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112547%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112547%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112547%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/49981","outbound_label":"Repository record","outbound_source":"dc:identifier"},"source_record":{"url":"https://publications.rwth-aachen.de/oai2d?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Apublications.rwth-aachen.de%3A49981","prefix":"oai_dc"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Mertens, Peter René"]},{"key":"dc:creator","label":"Author","values":["Martinkus, Sandra"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2008"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22158"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Glomerulonephritis","Mesangiale Immunglobulin-A-Glomerulonephritis","Zellzyklus","Grün fluoreszierendes Protein","Transkriptionsfaktor","Medizin","YB-1","NLS","NES","Roscovitin","Leptomycin B","roscovitine"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/49981","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112547%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["As a DNA- and RNA binding protein the cold-shock protein YB-1 serves multiple functions in the nucleus and cytoplasm, e.g. regulating transcription, RNA-processing, -translation and –storage. In the present study we examined the expression and localisation pattern of YB-1 in various models of glomerular diseases. Furthermore we determined protein regions involved in the regulation of YB-1 localisation. In glomeruli of healthy rat kidneys YB-1 is detected exclusively in the nucleus by means of immunohistochemistry with two different antibodies against YB-1. In the course of the Ant-Thy 1.1- nephritis YB-1 changes its localisation and expression pattern. Within one day YB-1 localizes to the perinuclear region of cells within all glomeruli . In the course of the disease the strongest cytoplasmic YB-1 signal coincided with the peak mesangial cell activation/proliferation between days 4 and 6 and was detected in a mesangial distribution pattern. With resolution of the disease at day 31 with complete morphological restitution was associated with YB-1 relocalisation to the nucleus. In the course of different other models of rat glomerular disease YB-1 remained nuclear. In the second part of the study we examined YB-1 localisation in the in vitro model of proliferating rat mesangial cells, which are activated in cell culture conditions. In these cells endogenous YB-1 as well as transfected GFP-YB-1-proteins was detected in the cytoplasm. Using cell cycle inhibitors we tried to arrest the rat mesangial cells. Only after treatment with roscovitine, a specific CDK- inhibitor, YB-1 translocated into the nucleus. Cloning various deletion construct of YB-1 with a fluorescent tag we identified three nuclear localisation signals (NLS: AS 185-194, AS 149-156, AS 276-292) and two cytoplasmic localisation signals or nuclear export signals ( ZLS: AS 1-57, AS 52-146). Experiments using leptomycin B as an inhibitor of the CRM1 dependent nuclear export could reveal a CRM-1 independent export of YB-1. In summary these results document an increased expression and translocation of YB-1 in mesangial cells in the course of glomerulonephritis, therefore YB-1 has pivotal role coordinating inflammatory processes in glomerular disease."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 112 S. : Ill., graph. Darst. (2008). = Aachen, Techn. Hochsch., Diss., 2008"]},{"key":"dc:title","label":"Title","values":["Subzelluläre Lokalisation des Y-box-Proteins-1 (YB-1) in Mesangialzellen und Charakterisierung der dafür verantwortlichen Proteindomänen"]}]}],"canonical_facts":{"dc:contributor":["Mertens, Peter René"],"dc:coverage":["DE"],"dc:creator":["Martinkus, Sandra"],"dc:date":["2008"],"dc:description":["As a DNA- and RNA binding protein the cold-shock protein YB-1 serves multiple functions in the nucleus and cytoplasm, e.g. regulating transcription, RNA-processing, -translation and –storage. 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In the second part of the study we examined YB-1 localisation in the in vitro model of proliferating rat mesangial cells, which are activated in cell culture conditions. In these cells endogenous YB-1 as well as transfected GFP-YB-1-proteins was detected in the cytoplasm. Using cell cycle inhibitors we tried to arrest the rat mesangial cells. Only after treatment with roscovitine, a specific CDK- inhibitor, YB-1 translocated into the nucleus. Cloning various deletion construct of YB-1 with a fluorescent tag we identified three nuclear localisation signals (NLS: AS 185-194, AS 149-156, AS 276-292) and two cytoplasmic localisation signals or nuclear export signals ( ZLS: AS 1-57, AS 52-146). Experiments using leptomycin B as an inhibitor of the CRM1 dependent nuclear export could reveal a CRM-1 independent export of YB-1. In summary these results document an increased expression and translocation of YB-1 in mesangial cells in the course of glomerulonephritis, therefore YB-1 has pivotal role coordinating inflammatory processes in glomerular disease."],"dc:identifier":["https://publications.rwth-aachen.de/record/49981","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112547%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22158"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 112 S. : Ill., graph. Darst. (2008). = Aachen, Techn. 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