Matches in SemOpenAlex for { <https://semopenalex.org/work/W1996501345> ?p ?o ?g. }
- W1996501345 endingPage "277" @default.
- W1996501345 startingPage "270" @default.
- W1996501345 abstract "Abstract The transcription factor PU.1 plays a pivotal role in normal myeloid differentiation. PU.1−/− mice exhibit a complete block in myeloid differentiation. Heterozygous PU.1 mutations were reported in some patients with acute myeloid leukemia (AML), but not in AML with translocation t(8;21), which gives rise to the fusion geneAML1-ETO. Here we report a negative functional impact of AML1-ETO on the transcriptional activity of PU.1. AML1-ETO physically binds to PU.1 in t(8;21)+ Kasumi-1 cells. AML1-ETO binds to the β3β4 region in the DNA-binding domain of PU.1 and displaces the coactivator c-Jun from PU.1, thus down-regulating the transcriptional activity of PU.1. This physical interaction of AML1-ETO and PU.1 did not abolish the DNA-binding capacity of PU.1. AML1-ETO down-regulates the transactivation capacity of PU.1 in myeloid U937 cells, and the expression levels of PU.1 target genes in AML French-American-British (FAB) subtype M2 patients with t(8;21) were lower than in patients without t(8;21). Conditional expression of AML1-ETO causes proliferation in mouse bone marrow cells and inhibits antiproliferative function of PU.1. Overexpression of PU.1, however, differentiates AML1-ETO–expressing Kasumi-1 cells to the monocytic lineage. Thus, the function of PU.1 is down-regulated by AML1-ETO in t(8;21) myeloid leukemia, whereas overexpression of PU.1 restores normal differentiation." @default.
- W1996501345 created "2016-06-24" @default.
- W1996501345 creator A5021995072 @default.
- W1996501345 creator A5031734936 @default.
- W1996501345 creator A5033935778 @default.
- W1996501345 creator A5039005787 @default.
- W1996501345 creator A5039428434 @default.
- W1996501345 creator A5064722914 @default.
- W1996501345 creator A5065813780 @default.
- W1996501345 creator A5084400799 @default.
- W1996501345 date "2003-01-01" @default.
- W1996501345 modified "2023-10-18" @default.
- W1996501345 title "The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemia" @default.
- W1996501345 cites W1483582136 @default.
- W1996501345 cites W1489323849 @default.
- W1996501345 cites W1502074492 @default.
- W1996501345 cites W1524671781 @default.
- W1996501345 cites W1553385236 @default.
- W1996501345 cites W155663183 @default.
- W1996501345 cites W1599437019 @default.
- W1996501345 cites W1739103212 @default.
- W1996501345 cites W1820527096 @default.
- W1996501345 cites W1875148047 @default.
- W1996501345 cites W1885533743 @default.
- W1996501345 cites W1945687446 @default.
- W1996501345 cites W1964103753 @default.
- W1996501345 cites W1974612283 @default.
- W1996501345 cites W1974937526 @default.
- W1996501345 cites W1980771751 @default.
- W1996501345 cites W1985177466 @default.
- W1996501345 cites W1994987603 @default.
- W1996501345 cites W1996234002 @default.
- W1996501345 cites W2003617876 @default.
- W1996501345 cites W2004450968 @default.
- W1996501345 cites W2008079574 @default.
- W1996501345 cites W201291539 @default.
- W1996501345 cites W2033594965 @default.
- W1996501345 cites W2053208432 @default.
- W1996501345 cites W2054210423 @default.
- W1996501345 cites W2059340669 @default.
- W1996501345 cites W2068728784 @default.
- W1996501345 cites W2074333479 @default.
- W1996501345 cites W2080991719 @default.
- W1996501345 cites W2085033687 @default.
- W1996501345 cites W2091754665 @default.
- W1996501345 cites W2096008106 @default.
- W1996501345 cites W2096757412 @default.
- W1996501345 cites W2100088478 @default.
- W1996501345 cites W2108404291 @default.
- W1996501345 cites W2109841776 @default.
- W1996501345 cites W2113086962 @default.
- W1996501345 cites W2118161431 @default.
- W1996501345 cites W2119266042 @default.
- W1996501345 cites W2122968144 @default.
- W1996501345 cites W2123480703 @default.
- W1996501345 cites W2124597426 @default.
- W1996501345 cites W2130524213 @default.
- W1996501345 cites W2132749685 @default.
- W1996501345 cites W2138483214 @default.
- W1996501345 cites W2159374958 @default.
- W1996501345 cites W2161743101 @default.
- W1996501345 cites W2165787335 @default.
- W1996501345 cites W2168524285 @default.
- W1996501345 cites W2266988004 @default.
- W1996501345 cites W2279275424 @default.
- W1996501345 cites W2286150378 @default.
- W1996501345 cites W2323808648 @default.
- W1996501345 cites W4234755708 @default.
- W1996501345 cites W4253702721 @default.
- W1996501345 cites W4255146022 @default.
- W1996501345 cites W4312790597 @default.
- W1996501345 cites W4385970358 @default.
- W1996501345 doi "https://doi.org/10.1182/blood-2002-04-1288" @default.
- W1996501345 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12393465" @default.
- W1996501345 hasPublicationYear "2003" @default.
- W1996501345 type Work @default.
- W1996501345 sameAs 1996501345 @default.
- W1996501345 citedByCount "220" @default.
- W1996501345 countsByYear W19965013452012 @default.
- W1996501345 countsByYear W19965013452013 @default.
- W1996501345 countsByYear W19965013452014 @default.
- W1996501345 countsByYear W19965013452015 @default.
- W1996501345 countsByYear W19965013452016 @default.
- W1996501345 countsByYear W19965013452017 @default.
- W1996501345 countsByYear W19965013452018 @default.
- W1996501345 countsByYear W19965013452019 @default.
- W1996501345 countsByYear W19965013452020 @default.
- W1996501345 countsByYear W19965013452021 @default.
- W1996501345 countsByYear W19965013452022 @default.
- W1996501345 countsByYear W19965013452023 @default.
- W1996501345 crossrefType "journal-article" @default.
- W1996501345 hasAuthorship W1996501345A5021995072 @default.
- W1996501345 hasAuthorship W1996501345A5031734936 @default.
- W1996501345 hasAuthorship W1996501345A5033935778 @default.
- W1996501345 hasAuthorship W1996501345A5039005787 @default.
- W1996501345 hasAuthorship W1996501345A5039428434 @default.
- W1996501345 hasAuthorship W1996501345A5064722914 @default.
- W1996501345 hasAuthorship W1996501345A5065813780 @default.