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1دورية أكاديمية
المؤلفون: B Metzroth, T Marx, M Linnig, B Fleischer, Bernhard Metzroth, Tim Marx, Monika Linnig, Bernhard Fleischer
المساهمون: The Pennsylvania State University CiteSeerX Archives
الوصف: enterotoxin B deletion mutant proteins. superantigenic activity of staphylococcal Concomitant loss of conformation and
وصف الملف: application/pdf
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المؤلفون: Bernhard Horsthemke, Katherine M. Call, Bernhard Metzroth, Bernhard Zabel, Gabriele Senger, Lisa Davis, Uwe Claussen, Thomas B. Shows, David E. Housman, Hermann-Josef Lüdecke
المصدر: Genomics. 10(3)
مصطلحات موضوعية: Genes, Wilms Tumor, Translocation Breakpoint, Locus (genetics), Chromosomal translocation, Chromosomal rearrangement, Biology, Hybrid Cells, Wilms Tumor, Translocation, Genetic, Mice, Gene mapping, Genetics, medicine, Animals, Humans, Lymphocytes, Chromosomes, Human, Pair 14, Chromosomes, Human, Pair 11, Breakpoint, Chromosome, Wilms' tumor, DNA, medicine.disease, Molecular biology, Kidney Neoplasms, Chromosome Deletion
الوصف: A sporadic Wilms tumor, WT-21, with an (11;14)-(p13;q23) reciprocal translocation has been identified. The translocation is found in tumor cells, but not in the patients' circulating lymphocytes. Molecular analysis of somatic cell hybrids segregating the derivative translocation chromosomes reveals a submicroscopic interstitial deletion at the translocation breakpoint, as well as a cytologically undetectable interstitial deletion in the nontranslocation chromosome 11, resulting in a homozygous deletion in 11p13. Pulsed-field gel analysis of tumor DNA indicates that the two deletions are indistinguishable, and the homozygously deleted region is less than 875 kb. The homozygously deleted regions of three other sporadic Wilms tumors overlap with the deleted region in WT-21, and the candidate cDNA clone for the 11p13 Wilms tumor gene described by Call et al. (Cell 60, 509–520, 1990) is included in the deleted region. These findings strengthen previous conclusions regarding the obligate location for the 11p13 WT locus and support the suggestion that the Wilms tumor gene has been cloned.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8b33c7a7036613f627cb8cd2736c0128Test
https://pubmed.ncbi.nlm.nih.gov/1653761Test -
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المصدر: Cell. 50:215-225
مصطلحات موضوعية: Transposable element, Transcription, Genetic, Cellular differentiation, Biology, General Biochemistry, Genetics and Molecular Biology, Exon, Suppression, Genetic, Complementary DNA, Animals, Coding region, Amino Acid Sequence, Cloning, Molecular, Gene, Genetics, Base Sequence, Alternative splicing, Protein primary structure, Cell Differentiation, DNA, Neoplasms, Experimental, Cell biology, Genes, DNA Transposable Elements, Drosophila, Genes, Lethal, Chromosome Deletion, Cell Division
الوصف: We have previously cloned lethal(2)giant larvae , a tumor-suppressor gene of Drosophila that normally controls cell proliferation and/or differentiation in the optic centers of the brain and the imaginal discs. Here we describe the structure of the I(2)gl gene as determined by sequencing genomic and cDNA clones. The structure of the cDNAs indicates the use of alternative splicing, either in the 5′ untranslated exons or in the 3′ coding exons. Thus the gene encodes two putative proteins of 1161 and 708 amino acids, p127 and p78, respectively, differing at their C termini. A 3′-truncated I(2)gl transposon that leaves the coding sequence of p78 intact but deletes 141 residues of p127 was capable of suppressing tumor formation in I(2)gl -deficient animals. These results suggest that the putative p78 protein is effective in controlling cell proliferation and/or differentiation.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::366f2d089ce6aac0c9a14c490923ea8cTest
https://doi.org/10.1016/0092-8674Test(87)90217-0
