Characterization of the human myeloid cell nuclear differentiation antigen gene promoter

Pharmacogenomics of responsiveness to interferon IFN-β treatment in multiple sclerosis: A genetic screen of 100 type I interferon-inducible genes

“…Further investigation of these and other genes involved in this specific pathway should elucidate whether, at any rate, this is the main determinant of response to type I IFN treatment. In any case it is remarkable that, despite numerous reports highlighting differences in cytokine expression profiles after IFN-␤ treatment in MS patients, 53,54 in our study not a single cytokine (receptor) gene, out of about 10 scrutinized, contained polymorphisms showing association with response. Pending further investigation, this suggests that altered regulation of cytokine expression on IFN treatment could be merely phenotypic.…”

The murine homolog of the HIN 200 family, Ifi 204, is constitutively expressed in myeloid cells and selectively induced in the monocyte/macrophage lineage

“…The p204 expression pattern resembles that of the human gene MNDA, which is constitutively expressed in cells within the myeloid lineage (i.e., granulocytes and monocytes) [27][28][29] and up-regulated by IFNs in monocytes; it differs inasmuch as p204 is expressed in monocytes and megakaryocytes, and is up-regulated by a wider spectrum of inducers such as IFN-␣, IFN-␥, LPS, and poly rI:rC. Finally, it is in variance with that of the IFI16 protein, whose expression is not restricted to hematopoietic cells [30,31].…”

“…In the 5' flanking sequence of MNDA, several Myb and Ets binding elements are present, including an Ets-related PU.1 binding site known to be expressed specifically in M and B cells [28,34,35]. Analysis of the myeloid-specific CD11b promoter has indeed provided evidence that binding of both the PU.1 and the Sp1 transcription factor are required for its lineage-specific expression [36,37].…”

MNDA dimerizes through a complex motif involving an N‐terminal basic region

“…MNDA is up-regulated specifically by interferon a in nearly all cells that exhibit constitutive expression. The MNDA promoter [5] contains several consensus regulatory elements, including c-myb [6][7][8][9], PU.l [10][11][12][13][14][15][16][17][18], ISRE [19] and Spl [20][21][22][23], consistent with MNDA's myelomonocytic lineage-specific expression and regulation by interferon a. Analysis of MNDAassociated proteins and assessment of the effects of MNDA expression on promoter activities of different genes has led to the proposal that MNDA plays a role in transcription regulation by influencing the actions of other transcription factors [24,25].…”