Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A fundamental problem in the identification and isolation of tumor suppressor and other growth-inhibiting genes is the loss of power of genetic complementation at the subchromosomal level. A direct genetic strategy was developed to isolate subchromosomal transferable fragments (STFs) from any chromosome, each containing a selectable marker within the human DNA, that could be transferred to any mammalian cell. As a test of the method, several overlapping STFs from 11p15 were shown to cause in vitro growth arrest of rhabdomyosarcoma cells. This activity mapped between the beta-globin and insulin genes.
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PMID:Tumor cell growth arrest caused by subchromosomal transferable DNA fragments from chromosome 11. 846 89

Tissue-specific alternative RNA splicing in human F1gamma pre-mRNA produces muscle- and nonmuscle-type isoforms. Muscle-specific exclusion of exon 9 of the F1gamma gene is cell-specifically induced by acidic treatment of human fibrosarcoma HT1080 and rhabdomyosarcoma KYM-1 cells. We constructed an F1gamma minigene containing parts of exon 8, intron 8, and exon 9 of the human F1gamma gene and then analyzed a negative factor that inhibited inclusion of exon 9 via an in vitro splicing assay using acid-stimulated HT1080 cell nuclear extract. In vitro splicing of the F1gamma minigene, similarly to the beta-globin minigene used as a control, was observed in HeLa cell nuclear extract. Next, we performed supplemental experiments using HeLa and HT1080 cell nuclear extracts. The splicing reaction of the F1gamma minigene was specifically inhibited by supplementation with nuclear extract from acid-stimulated HT1080 cells, whereas that of human beta-globin was not inhibited. These results indicated that acidic stimulation induced a negative factor that blocked inclusion of alternatively spliced exon in the F1gamma minigene in vitro, and a regulatory factor acted in a sequence-specific manner for muscle-specific alternative splicing in F1gamma pre-mRNA.
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PMID:Acidic stimulation induces a negative regulatory factor that affects alternative exon selection in vitro in human ATP synthase gamma-subunit pre-mRNA. 979 20