tsg101: a novel tumor susceptibility gene isolated by controlled homozygous functional knockout of allelic loci in mammalian cells
Article Abstract:
The spontaneous cell proliferation of cancerous tissue is caused by the abnormal regulation of stathmin due to the effects of the tsg101 gene. This process was investigated by isolating tsg101 using antisense codons of ribonucleic acid. tsg101 was cloned in a petri dish and was inoculated in lab rats. The resulting tumor outgrowths showed that tsg101 triggers a faulty metabolic reaction that abnormally increases stathmin causing uncontrolled cell differentiation. The elimination of the transactivating promoter gene was effective in reversing tumor genesis.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
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The TSG101 tumor susceptibility gene is located in chromosome 11 band p15 and is mutated in human breast cancer
Article Abstract:
The human homolog TSG101 has been isolated and mapped to chromosome 11, bands 15.1-15.2, a region showing loss of heterozygosity in several human malignancies, especially breast cancers. The homolog was observed to mutate at high frequency in human breast cancer. No TSG101 defects were observed in matched normal breast tissue from breast cancer patients. Results indicate that defects in TSG101 occur during breast cancer tumorigenesis and/or progression.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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Surprises at the 3' end of prokaryotic RNA
Article Abstract:
Polyadenylation at the 3' end of RNA made in prokaryotic cells is involved in regulating the decay of mRNA, similar to the process in eukaryotic cells. Studies of E. coli show that cells with normal pcnB gene undergo RNA decay initiated by ribonuclease E. In cells with mutant pcnB, however, RNA degradation is retarded.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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