Yolanda de Diego Otero, Cathy E. Bakker, Prawien Raghoe, Lies-Anne W.F.M. Severijnen, Andre Hoogeveen, Ben A. Oostra, Rob Willemsen
{"title":"小鼠胚胎发育过程中FMRP、FXR1P和FXR2P的免疫细胞化学特征","authors":"Yolanda de Diego Otero, Cathy E. Bakker, Prawien Raghoe, Lies-Anne W.F.M. Severijnen, Andre Hoogeveen, Ben A. Oostra, Rob Willemsen","doi":"10.1002/1438-826X(200005)1:1<28::AID-GNFD28>3.0.CO;2-F","DOIUrl":null,"url":null,"abstract":"<p>The absence of the <i>FMR1</i> (fragile X mental retardation gene 1) gene product, protein FMRP (fragile X mental retardation protein) is causing the fragile X syndrome. FMRP, together with two homologues, called FXR1P and FXR2P, belongs to a small family of RNA-binding proteins (FXR proteins). The precise physiological function of the FXR proteins is unknown, but a role in mRNA transport has been suggested. In the present study, we have performed immunolocalization of these proteins during the embryonic development of the mouse to get more insight in their physiological function. All three proteins are expressed during mouse embryonic development, however, the pattern and intensity varies for each protein at the different developmental stages. During early development, the distribution of the Fxr proteins exhibits high similarities, however, during late development and in the neonate a more differential expression is observed especially in some non-neural tissues. The results of this descriptive study are discussed in relation to the pathogenesis of the fragile X syndrome. </p>","PeriodicalId":100573,"journal":{"name":"Gene Function & Disease","volume":"1 1","pages":"28-37"},"PeriodicalIF":0.0000,"publicationDate":"2000-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/1438-826X(200005)1:1<28::AID-GNFD28>3.0.CO;2-F","citationCount":"33","resultStr":"{\"title\":\"Immunocytochemical characterization of FMRP, FXR1P and FXR2P during embryonic development in the mouse\",\"authors\":\"Yolanda de Diego Otero, Cathy E. Bakker, Prawien Raghoe, Lies-Anne W.F.M. Severijnen, Andre Hoogeveen, Ben A. Oostra, Rob Willemsen\",\"doi\":\"10.1002/1438-826X(200005)1:1<28::AID-GNFD28>3.0.CO;2-F\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>The absence of the <i>FMR1</i> (fragile X mental retardation gene 1) gene product, protein FMRP (fragile X mental retardation protein) is causing the fragile X syndrome. FMRP, together with two homologues, called FXR1P and FXR2P, belongs to a small family of RNA-binding proteins (FXR proteins). The precise physiological function of the FXR proteins is unknown, but a role in mRNA transport has been suggested. In the present study, we have performed immunolocalization of these proteins during the embryonic development of the mouse to get more insight in their physiological function. All three proteins are expressed during mouse embryonic development, however, the pattern and intensity varies for each protein at the different developmental stages. During early development, the distribution of the Fxr proteins exhibits high similarities, however, during late development and in the neonate a more differential expression is observed especially in some non-neural tissues. The results of this descriptive study are discussed in relation to the pathogenesis of the fragile X syndrome. </p>\",\"PeriodicalId\":100573,\"journal\":{\"name\":\"Gene Function & Disease\",\"volume\":\"1 1\",\"pages\":\"28-37\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2000-05-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/1438-826X(200005)1:1<28::AID-GNFD28>3.0.CO;2-F\",\"citationCount\":\"33\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gene Function & Disease\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/1438-826X%28200005%291%3A1%3C28%3A%3AAID-GNFD28%3E3.0.CO%3B2-F\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene Function & Disease","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/1438-826X%28200005%291%3A1%3C28%3A%3AAID-GNFD28%3E3.0.CO%3B2-F","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Immunocytochemical characterization of FMRP, FXR1P and FXR2P during embryonic development in the mouse
The absence of the FMR1 (fragile X mental retardation gene 1) gene product, protein FMRP (fragile X mental retardation protein) is causing the fragile X syndrome. FMRP, together with two homologues, called FXR1P and FXR2P, belongs to a small family of RNA-binding proteins (FXR proteins). The precise physiological function of the FXR proteins is unknown, but a role in mRNA transport has been suggested. In the present study, we have performed immunolocalization of these proteins during the embryonic development of the mouse to get more insight in their physiological function. All three proteins are expressed during mouse embryonic development, however, the pattern and intensity varies for each protein at the different developmental stages. During early development, the distribution of the Fxr proteins exhibits high similarities, however, during late development and in the neonate a more differential expression is observed especially in some non-neural tissues. The results of this descriptive study are discussed in relation to the pathogenesis of the fragile X syndrome.