{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:62560"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:62560","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Gene deletion and functional analysis of Fetuin-B","abstract":"This study aimed at elucidating the physiological function of the serum protein fetuin-B and comparing it with its closest family member fetuin-A. Fetuin-A is known to be an inhibitor of calcium and phosphate precipitation in vivo. This has been shown in a fetuin-A-deficient animal model. In this study, the serum protein fetuin-B was deleted in an animal model to analyze its effect on the organism. The analysis of the fetuin-B-deficient mice revealed that fetuin-B was essential for fertilization. Female fetuin-B-deficient mice failed to produce any offspring when mated with any genotype. Heterozygous fetuin-B-deficient female mice and males of any genotype were reproductive, however. The main finding of this study was that oocytes derived from naturally mated fetuin-B-deficient female mice did not reveal any fertilization characteristics and did not develop to two-cell pre-implantation embryos in vitro, indicating a fertilization defect. It remains to be clarified whether fetuin-B is required as a structural, a catalytic, or a transport protein. In this study a novel target for fertilization control was identified: fetuin-B. Further characterization of the fetuin-B-deficient mice did not reveal any abnormalities with regard to their anatomy, morphology, physiological parameters or metabolic functions. It remains to be studied if the fetuin-B-deficient mice develop disease when challenged or stressed. Fetuin-B was cloned and expressed eukaryotically as a recombinant fusion protein. Functional in vitro assays performed with the purified recombinant fetuin-B showed that it could not compensate for fetuin-A deficiency, as shown by their distinct calcium phosphate precipitation inhibiting potential. As for the fetuin-A- and fetuin-B-deficient animal models, both exhibit distinct phenotypes and differ completely in their most prominent phenotypes: fetuin-A deficiency leads to ectopic calcification, while fetuin-B deficiency leads to female infertility. The data provided by this study thus clearly suggests that the fetuin-family members have distinct functions in vivo.","abstract_html":"This study aimed at elucidating the physiological function of the serum protein fetuin-B and comparing it with its closest family member fetuin-A. Fetuin-A is known to be an inhibitor of calcium and phosphate precipitation in vivo. This has been shown in a fetuin-A-deficient animal model. In this study, the serum protein fetuin-B was deleted in an animal model to analyze its effect on the organism. The analysis of the fetuin-B-deficient mice revealed that fetuin-B was essential for fertilization. Female fetuin-B-deficient mice failed to produce any offspring when mated with any genotype. Heterozygous fetuin-B-deficient female mice and males of any genotype were reproductive, however. The main finding of this study was that oocytes derived from naturally mated fetuin-B-deficient female mice did not reveal any fertilization characteristics and did not develop to two-cell pre-implantation embryos in vitro, indicating a fertilization defect. It remains to be clarified whether fetuin-B is required as a structural, a catalytic, or a transport protein. In this study a novel target for fertilization control was identified: fetuin-B. Further characterization of the fetuin-B-deficient mice did not reveal any abnormalities with regard to their anatomy, morphology, physiological parameters or metabolic functions. It remains to be studied if the fetuin-B-deficient mice develop disease when challenged or stressed. Fetuin-B was cloned and expressed eukaryotically as a recombinant fusion protein. Functional in vitro assays performed with the purified recombinant fetuin-B showed that it could not compensate for fetuin-A deficiency, as shown by their distinct calcium phosphate precipitation inhibiting potential. As for the fetuin-A- and fetuin-B-deficient animal models, both exhibit distinct phenotypes and differ completely in their most prominent phenotypes: fetuin-A deficiency leads to ectopic calcification, while fetuin-B deficiency leads to female infertility. The data provided by this study thus clearly suggests that the fetuin-family members have distinct functions in vivo.","abstract_has_math":false,"creators":["Wessling, Jennifer"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Jahnen-Dechent, Wilhelm"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2007,"date_issued":"2007","date_published":"2007","updated_at":"2026-07-30T19:43:28Z","subjects":["info:eu-repo/classification/ddc/570","Knockout <Molekulargenetik>","Fortpflanzung","Biowissenschaften, Biologie","Serumprotein","Infertilität","Oozyten","Befruchtung","Fetuin","Knockout","Reproduction","Serum protein","Infertility","Fertilization"],"languages":["eng"],"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-124124%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-124124%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-124124%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/62560","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Jahnen-Dechent, Wilhelm"]},{"key":"dc:creator","label":"Author","values":["Wessling, Jennifer"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2007"]},{"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-21053"]},{"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/570","Knockout <Molekulargenetik>","Fortpflanzung","Biowissenschaften, Biologie","Serumprotein","Infertilität","Oozyten","Befruchtung","Fetuin","Knockout","Reproduction","Serum protein","Infertility","Fertilization"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"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/62560","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-124124%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["This study aimed at elucidating the physiological function of the serum protein fetuin-B and comparing it with its closest family member fetuin-A. Fetuin-A is known to be an inhibitor of calcium and phosphate precipitation in vivo. This has been shown in a fetuin-A-deficient animal model. In this study, the serum protein fetuin-B was deleted in an animal model to analyze its effect on the organism. The analysis of the fetuin-B-deficient mice revealed that fetuin-B was essential for fertilization. Female fetuin-B-deficient mice failed to produce any offspring when mated with any genotype. Heterozygous fetuin-B-deficient female mice and males of any genotype were reproductive, however. The main finding of this study was that oocytes derived from naturally mated fetuin-B-deficient female mice did not reveal any fertilization characteristics and did not develop to two-cell pre-implantation embryos in vitro, indicating a fertilization defect. It remains to be clarified whether fetuin-B is required as a structural, a catalytic, or a transport protein. In this study a novel target for fertilization control was identified: fetuin-B. Further characterization of the fetuin-B-deficient mice did not reveal any abnormalities with regard to their anatomy, morphology, physiological parameters or metabolic functions. It remains to be studied if the fetuin-B-deficient mice develop disease when challenged or stressed. Fetuin-B was cloned and expressed eukaryotically as a recombinant fusion protein. Functional in vitro assays performed with the purified recombinant fetuin-B showed that it could not compensate for fetuin-A deficiency, as shown by their distinct calcium phosphate precipitation inhibiting potential. As for the fetuin-A- and fetuin-B-deficient animal models, both exhibit distinct phenotypes and differ completely in their most prominent phenotypes: fetuin-A deficiency leads to ectopic calcification, while fetuin-B deficiency leads to female infertility. The data provided by this study thus clearly suggests that the fetuin-family members have distinct functions in vivo."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University IV, 143 S. : Ill., graph. Darst. (2007). = Aachen, Techn. Hochsch., Diss., 2007"]},{"key":"dc:title","label":"Title","values":["Gene deletion and functional analysis of Fetuin-B"]}]}],"canonical_facts":{"dc:contributor":["Jahnen-Dechent, Wilhelm"],"dc:coverage":["DE"],"dc:creator":["Wessling, Jennifer"],"dc:date":["2007"],"dc:description":["This study aimed at elucidating the physiological function of the serum protein fetuin-B and comparing it with its closest family member fetuin-A. Fetuin-A is known to be an inhibitor of calcium and phosphate precipitation in vivo. This has been shown in a fetuin-A-deficient animal model. In this study, the serum protein fetuin-B was deleted in an animal model to analyze its effect on the organism. The analysis of the fetuin-B-deficient mice revealed that fetuin-B was essential for fertilization. Female fetuin-B-deficient mice failed to produce any offspring when mated with any genotype. Heterozygous fetuin-B-deficient female mice and males of any genotype were reproductive, however. The main finding of this study was that oocytes derived from naturally mated fetuin-B-deficient female mice did not reveal any fertilization characteristics and did not develop to two-cell pre-implantation embryos in vitro, indicating a fertilization defect. It remains to be clarified whether fetuin-B is required as a structural, a catalytic, or a transport protein. In this study a novel target for fertilization control was identified: fetuin-B. Further characterization of the fetuin-B-deficient mice did not reveal any abnormalities with regard to their anatomy, morphology, physiological parameters or metabolic functions. It remains to be studied if the fetuin-B-deficient mice develop disease when challenged or stressed. Fetuin-B was cloned and expressed eukaryotically as a recombinant fusion protein. Functional in vitro assays performed with the purified recombinant fetuin-B showed that it could not compensate for fetuin-A deficiency, as shown by their distinct calcium phosphate precipitation inhibiting potential. As for the fetuin-A- and fetuin-B-deficient animal models, both exhibit distinct phenotypes and differ completely in their most prominent phenotypes: fetuin-A deficiency leads to ectopic calcification, while fetuin-B deficiency leads to female infertility. The data provided by this study thus clearly suggests that the fetuin-family members have distinct functions in vivo."],"dc:identifier":["https://publications.rwth-aachen.de/record/62560","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-124124%22"],"dc:language":["eng"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-21053"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University IV, 143 S. : Ill., graph. Darst. (2007). = Aachen, Techn. 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