| pubmed-article:1705831 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0870134 | lld:lifeskim |
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| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0012888 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1998793 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1511938 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C1516960 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
| pubmed-article:1705831 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:1705831 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:1705831 | pubmed:dateCreated | 1991-4-17 | lld:pubmed |
| pubmed-article:1705831 | pubmed:abstractText | These studies aimed to determine the expression and functional role of c-myb in erythroid progenitors with different cycling activities. In the first series of experiments the erythroid burst-forming unit (BFU-E) and colony-forming unit (CFU-E) populations from adult peripheral blood (PB), bone marrow (BM), and embryonic-fetal liver (FL) were treated with either c-myb antisense oligomers or 3H-thymidine (3H-TdR). A direct correlation was always observed between the inhibitory effect of anti-myb oligomers and the level of cycling activity. Thus, the inhibitory effect of antisense c-myb on the number of BFU-E colonies was 28.3% +/- 15.8% in PB, 53.4% +/- 9.3% in BM, and 68.2% +/- 24.5% in FL. Both adult and embryonic CFU-E were markedly inhibited (73.2% +/- 10.4% and 74.2% +/- 12.7%). Using highly purified PB progenitors, we observed a similar pattern, although with slightly lower inhibitory effects. In the 3H-TdR suicide assay the killing index of BFU-E was 8.9% +/- 4.2% in PB, 29.4% +/- 6.5% in BM, and 40.1% +/- 9.6% in FL. The values for adult and embryonic CFU-E were 55.7% +/- 7.9% and 60.98% +/- 6.6%, respectively. We then investigated the kinetics of c-myb mRNA level during the erythroid differentiation of highly purified adult PB and FL BFU-E, as evaluated in liquid-phase culture by reverse transcription-polymerase chain reaction. Adult erythroid precursors showed a gradual increase of c-myb mRNA from day 4 through day 8 of culture and a sharp decrease at later times, whereas the expression of c-myb mRNA and protein in differentiation embryonic precursors peaked 2 days earlier. In both cases, c-myb mRNA level peaked at the CFU-E stage of differentiation. Finally, highly purified adult PB BFU-E were stimulated into cycling by a 3-day treatment with interleukin-3 in liquid phase: both the sensitivity to c-myb antisense oligomers and the 3H-TdR suicide index showed a gradual, strictly parallel increase. Under the same experimental conditions a progressive increase of the mRNA level of DNA polymerase alpha was observed. These observations suggest that in early erythroid differentiation c-myb activation is associated with the progression of progenitors into the S phase of the cell cycle, as well as to the synthesis of DNA polymerase alpha. | lld:pubmed |
| pubmed-article:1705831 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1705831 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1705831 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:1705831 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1705831 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:1705831 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:FossatiCC | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:PeschleCC | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:CalabrettaBB | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:PelosiEE | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:GewirtzA MAM | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:VenturelliDD | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:ValtieriMM | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:LabbayeCC | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:MattiaGG | lld:pubmed |
| pubmed-article:1705831 | pubmed:author | pubmed-author:CaréAA | lld:pubmed |
| pubmed-article:1705831 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1705831 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:1705831 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:1705831 | pubmed:geneSymbol | c-myb | lld:pubmed |
| pubmed-article:1705831 | pubmed:geneSymbol | c-myc | lld:pubmed |
| pubmed-article:1705831 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1705831 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1705831 | pubmed:pagination | 1181-90 | lld:pubmed |
| pubmed-article:1705831 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:1705831 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1705831 | pubmed:articleTitle | Antisense myb inhibition of purified erythroid progenitors in development and differentiation is linked to cycling activity and expression of DNA polymerase alpha. | lld:pubmed |
| pubmed-article:1705831 | pubmed:affiliation | Department of Hematology-Oncology, Istituto Superiore di Sanità, Rome, Italy. | lld:pubmed |
| pubmed-article:1705831 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1705831 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:1705831 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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