期刊
JOURNAL OF IMMUNOLOGY
卷 169, 期 12, 页码 6664-6667出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.12.6664
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- NCI NIH HHS [CA 68485] Funding Source: Medline
- NIAID NIH HHS [AI 44924] Funding Source: Medline
- NIDDK NIH HHS [DK20593] Funding Source: Medline
Using a transgenic approach, 4 analyzed the contribution of introns located within the IFN-gamma gene and distal regulatory regions to IFN-gamma gene expression. Intron 1 and 3 from the IFN-gamma gene displayed strong enhancer activity. This activity appeared to be dependent upon integration into the genome but resulted in a loss of Th1 selectivity. We also found that distal regulatory elements are not required for high level expression of the human IFN-gamma gene, but rather for cell lineage-specific expression. An 8.6-kb human IFN-gamma transgene was sufficient to yield high level expression but a 191-kb IFN-gamma transgene with similar to90 kb of flanking 5' and 3' sequence was necessary to achieve both high level and Th1 selective expression of human IFN-gamma.
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