Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.22.61 (caspase-8)
 6,833 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the genomic sequence of multicellular organisms such as Caenorhabditis elegans, Drosophila melanogaster, and Homo sapiens completed and others to be finished in the near future, the focus has shifted from accumulating sequence information to the prediction and analysis of genes within the completed genomes. Unfortunately, presently available computer programs do not always accurately predict gene structure such as mRNA and translation start sites or intron/exon boundaries. The only way to be certain about a gene's structure is to isolate and characterize its cDNA. Since the screening of libraries is a time-consuming, labor-intensive process that sometimes fails to yield the desired clone, we searched for faster, more efficient ways to isolate cDNAs. In this study, we describe two methods for amplification and isolation of cDNAs from plasmid libraries that requires no hybridization (MACH). With the polymerase chain reaction-based MACH-2 protocol, we present a strategy that requires little DNA sequence information to selectively isolate the longest cDNA variant from plasmid libraries in about 3 days. Our protocols were used to isolate cDNAs for the Drosophila activin and follistatin genes.
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PMID:Isolation of Drosophila activin and follistatin cDNAs using novel MACH amplification protocols. 1209 82

Activin has a wide variety of biological functions, including the regulation of cell proliferation and inhibition of tumor cells. We have studied whether activin regulates apoptosis by investigating the effects of activin A on cell proliferation, cell cycle, apoptosis, apoptosis-related gene expression, and caspase activity in SNU-16 cells. Activin A significantly inhibited DNA synthesis and growth suppression in a time-dependent manner in SNU-16 cells. Apoptosis fraction was increased at cell cycle with an accompanying DNA fragmentation. Activin A resulted in a significant time-dependent decrease in Bcl-2 mRNA levels and increase in caspase-3 mRNA levels in SNU-16 cells. No significant difference was observed in Bax mRNA levels. Exposure of cells to activin A induced caspase-3, -8 and -9 activation in SNU-16 cells. Furthermore, co-treatment of activin with the pan-caspase inhibitor Z-VAD-FMK, caspase-3 inhibitor Z-DEVE-FMK, caspase-8 inhibitor Z-IETD-FMK, and caspase-9-inhibitor Z-LEHD-FMK blocked apoptosis of SNU-16 cells. Taken together, our results revealed that activin inhibits the growth of SNU-16 cells by inducing apoptosis through caspase activation.
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PMID:Cell growth regulation through apoptosis by activin in human gastric cancer SNU-16 cell lines. 1914 27