Literature DB >> 8021494

The A-myb gene is preferentially expressed in tonsillar CD38+, CD39-, and sIgM- B lymphocytes and in Burkitt's lymphoma cell lines.

J Golay1, E Erba, S Bernasconi, G Peri, M Introna.   

Abstract

The A-myb gene is structurally related to the c-mby proto-oncogene, a transcription factor involved in the regulation of hemopoietic proliferation and differentiation. Recent evidence has shown that A-myb also functions as a transcriptional activator. We have previously demonstrated that A-myb RNA is not expressed in most mature human leukocytes at rest or after mitogenic or functional activation. We show here, by using cell sorting, PCR, and Western analyses that A-myb is most highly expressed in the subsets of human tonsillar B lymphocytes with the phenotypes CD38+, CD39-, and SIgM-. The preferential expression of A-myb in these populations was seen at both the RNA and protein levels. CD38 was consistently best at separating high from low A-myb-expressing cells, whereas other markers (CD10, 22, 23, 77, 11a, and 49d) did not correlate with A-myb expression. The CD38+ population expressing the highest levels of A-myb was shown to contain mostly cycling cells inasmuch as more than 95% were in the late G1, S, G2, and M phases of the cell cycle. In addition, A-myb expression always correlated with the percentage of cells in S/G2/M in the populations sorted with either CD38, CD39, or sIgM. Small resting tonsillar B lymphocytes induced to proliferate in vitro by several different polyclonal B cell activators did not, however, express detectable levels of A-myb, although these cells were demonstrated to express CD38 and enter the S/G2/M phases of the cell cycle. These data suggest that A-myb is a marker of in vivo-activated but not in vitro-activated B lymphocytes. Finally, A-myb was also found to be highly expressed in five of seven Burkitt's lymphoma lines and in none of three EBV lymphoblastoid cell lines. This finding is in agreement with the phenotype of the normal B cells that express high levels of A-myb in vivo and suggests that A-myb may be specifically induced within germinal center B cells.

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Year:  1994        PMID: 8021494

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  7 in total

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2.  Regulatory domains of the A-Myb transcription factor and its interaction with the CBP/p300 adaptor molecules.

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3.  Ectopic expression of A-myb in transgenic mice causes follicular hyperplasia and enhanced B lymphocyte proliferation.

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Journal:  Mol Cell Biol       Date:  1997-05       Impact factor: 4.272

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Authors:  C Gaillard; E Le Rouzic; C Créminon; B Perbal
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6.  The cytolytically inactive terminal complement complex activates endothelial cells to express adhesion molecules and tissue factor procoagulant activity.

Authors:  F Tedesco; M Pausa; E Nardon; M Introna; A Mantovani; A Dobrina
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7.  RFX2 is a candidate downstream amplifier of A-MYB regulation in mouse spermatogenesis.

Authors:  Gary C Horvath; Malathi K Kistler; W Stephen Kistler
Journal:  BMC Dev Biol       Date:  2009-12-09       Impact factor: 1.978

  7 in total

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