1998
DOI: 10.1002/jlb.64.5.608
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The murine homolog of the HIN 200 family, Ifi 204, is constitutively expressed in myeloid cells and selectively induced in the monocyte/macrophage lineage

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Cited by 38 publications
(43 citation statements)
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“…This is in contrast to MNDA, which is found in mature granulocytes and monocytes but not in lymphoid cells or undifferentiated myeloid cell lines (11,12). This expression pattern is similar to that of p204, which is constitutively expressed in myelomonocytic cells of the mouse (19).…”
Section: Structure and Expression Of The Hin-200 Proteinsmentioning
confidence: 75%
“…This is in contrast to MNDA, which is found in mature granulocytes and monocytes but not in lymphoid cells or undifferentiated myeloid cell lines (11,12). This expression pattern is similar to that of p204, which is constitutively expressed in myelomonocytic cells of the mouse (19).…”
Section: Structure and Expression Of The Hin-200 Proteinsmentioning
confidence: 75%
“…(12,13) This growth arrest is accompanied by cell differentiation, as suggested in vitro by the finding that myoblasts overexpressing p204 mature into myotubes (14) and in vivo by the finding that monocytes over-expressing p204 mature into peritoneal macrophages. (15) Finally, our results have demonstrated that expression of a mutant p204 devoid of both Rb-binding motifs interferes with the mouse cytomegalovirus (MCMV) multiplication cycle. The Ifi204 gene is indeed transcriptionally activated by MCMV infection and is required for its replication.…”
Section: Introduction Imentioning
confidence: 87%
“…Interestingly, the IFN-␥ expression level was increased 8.5-fold at 8 h postchallenge in the lungs of RacL11-challenged mice that had been immunized with KyA (Table 3). Since IFN-␥, IFN-␣, and lipopolysaccharide (LPS) induce IFI204 expression (68), it may be significant that IFN-␥ upregulated IFI204 29.7-fold in the lungs of RacL11-challenged mice that had been immunized with KyA 3 days prior to challenge. IFI16, a human homolog of IFI204, has been shown to interact with STING (stimulator of interferon genes), leading to the phosphorylation and nuclear translocation of IRF3 via the IFI16-STING-TBK signaling axis (69,70).…”
Section: Discussionmentioning
confidence: 99%