Molecular biology & medicine最新文献_第8页

Lymphomagenesis in Emu-myc transgenic mice does not require transgene rearrangement or mutation of myc exon 1. Emu-myc转基因小鼠的淋巴瘤发生不需要转基因重排或myc外显子1的突变。

Molecular biology & medicine Pub Date : 1989-12-01

E Webb, G Barri, S Cory, J M Adams

{"title":"Lymphomagenesis in Emu-myc transgenic mice does not require transgene rearrangement or mutation of myc exon 1.","authors":"E Webb, G Barri, S Cory, J M Adams","doi":"","DOIUrl":"","url":null,"abstract":"In most human Burkitt's lymphomas, translocation of the myc oncogene to an immunoglobulin locus is associated with loss of myc exon 1 or with mutations near its 3' border, a region where myc transcription is attenuated and translation of a larger myc polypeptide initiates. Emu-myc transgenic mice, which bear the three myc exons coupled to an immunoglobulin enhancer, provide a model for the development of such lymphomas, because their lymphomagenesis appears to require events other than expression of the transgene. To determine whether myc rearrangement or exon 1 mutation is a necessary tumorigenic event, we examined the transgene structure and myc exon 1 sequences in Emu-myc B lymphoid tumours. Southern blots revealed no transgene rearrangements in 20 of the lymphomas, and only two tumours showed amplification (2 to 5-fold). To search for exon 1 alterations, the exon 1 mRNA region was amplified from five tumours by polymerase chain reaction and sequenced, but no mutations were found. Hence, neither excision nor mutation of exon 1 is necessary to render myc tumorigenic. The sequence analysis across the exon 1-exon 2 boundary unexpectedly revealed an ambiguity in myc splicing that predicts a variant form of the larger myc polypeptide lacking a single amino acid residue.","PeriodicalId":77573,"journal":{"name":"Molecular biology & medicine","volume":"6 6","pages":"475-80"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13842378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Analysis of milk protein gene expression in transgenic mice. 乳蛋白基因在转基因小鼠中的表达分析。

Molecular biology & medicine Pub Date : 1989-12-01

J M Rosen, E Bayna, K F Lee

引用次数: 0

Embryonic stem cell culture and gene targeting in transgenic mice. 胚胎干细胞培养及转基因小鼠的基因靶向。

Molecular biology & medicine Pub Date : 1989-12-01

H Baribault, R Kemler

引用次数: 0

Detection of new mutation disease in man and mouse. 人、鼠新突变疾病的检测。

Molecular biology & medicine Pub Date : 1989-12-01

M Grompe, R A Gibbs, J S Chamberlain, C T Caskey

引用次数: 0

Genetic ablation in transgenic mice. 转基因小鼠的基因消融。

Molecular biology & medicine Pub Date : 1989-12-01

A Bernstein, M Breitman

{"title":"Genetic ablation in transgenic mice.","authors":"A Bernstein, M Breitman","doi":"","DOIUrl":"","url":null,"abstract":"The study of mammalian development has very quickly moved from a largely descriptive endeavour to one in which very precise mechanistic questions can now be formulated and answered. Undoubtedly, advances in this area have been the result of a strong foundation in experimental embryology, the application of molecular genetic techniques to the isolation and analysis of genes of developmental interest, and the ability to manipulate genetically the embryo through transgenic mouse technology. Perhaps the most dramatic illustration of the power of these new technologies is the potential ability to generate mice either that carry mutations in virtually any gene in the germ line through gene targeting in totipotent embryonic stem (ES) cells or that lack specific cell types through the genetic ablation technology reviewed here. Together, these two approaches have made it possible to knock out either a specific gene or a specific cell type in an intact animal and thus offer almost unlimited possibilities for addressing questions concerning the molecular and cellular biology of development. As well, animal models for various human diseases such as dwarfism, immunodeficiencies and demyelination can now be generated. It is clear that further refinements in both gene targeting and genetic ablation technologies are necessary before the full potential of either approach will be realized. Further development of conditional or inducible ablation strategies, coupled with a more precise definition of the cis-acting sequences, responsible for directing gene expression in fully differentiated and more primitive cells, will greatly broaden the range of questions that can be addressed by this approach.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77573,"journal":{"name":"Molecular biology & medicine","volume":"6 6","pages":"523-30"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13842382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transgenic mouse model of familial amyloidotic polyneuropathy. 家族性淀粉样变性多发性神经病转基因小鼠模型。

Molecular biology & medicine Pub Date : 1989-12-01 DOI: 10.2183/PJAB.63.344

S. Wakasugi, T. Inomoto, S. Yi, M. Naito, M. Uehira, T. Iwanaga, S. Maeda, Kimi Araki, Jun-ichi Miyazaki, Kiyoshi Takahashi, Kazunori Shimada, Ken-ichi Yamamura