| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
It has been shown that transport of mRNAs of Hepatitis B virus is inhibited by TAgRex, a Rex mutant, which dominantly inhibits Rev/Rex functions by sequestering the cellular cofactor(s). Moreover we showed that overexpression of hCRM1 partially restored the transport of HBV mRNA in contrast to the complete restoration of Rev/Rex functions. These results suggested that CRM1 analog, but not hCRM1 itself, is involved in the transport of HBV mRNAs. The purpose of the study this year is to identify the factor(s), particularly an analog of hCRM1, which may be involved in transport of HBV mRNAs. To clone it, we performed RT-PCR using primers of the hCRM1 genes with HeLa cDNA as template under the relaxed conditions. Sequence analysis of the PCR products indicated that all were hCRM1 itself. Next, we used cDNA prepared from astrocytoma cells, where Rev does not work efficiently, as template. It has been revealed that the amplified product had the sequence which has 89% similar to the hCRM1 cDNA at nucleotide level and 97% similar in amino acid sequence. We named this new gene as u-CRM1. Currently we are testing it to be involved in transport of HBV mRNAs.
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