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All - trans - retinoic acid upregulates CD 38 but not c - Kit antigens on human marrow CD 34 + cells without recruitment into cell cy
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IntroductionHuman CD38 is a 46-kD transmembrane glycoprotein that mediates multifunction activities, including signal transduction and cyclic ADP-ribose synthesis. It has been suggested that CD38 has an adhesion role, demonstrating that this molecule mediates weak cell binding to endothelium, probably through direct interaction with a ligand (CD31) located on the surface of endothelial cells. CD38 is physiologically down-regulated during myeloid cell differentiation, in that a significant proportion of normal precursor bone marrow cells (CD34+) express CD38 antigen, whereas it is only produced in small amount by normal mature polymorphonuclear cells [1]. Induction experiments indicate that all-trans retinoic acid (ATRA) is a potent and highly specific inducer of this antigen in myeloid cells. ATRA is notably able to upregulate CD38 antigen on human marrow CD34+ progenitor cells [2], but also on blast cells from the acute myeloblastic leukaemia (AML) cell line HL-60 [3], as well as on freshly isolated acute promyelocytic and AML cells when exposed to ATRA in vitro [4]and in vivo after oral treatment with ATRA [3].The gene super-family encoding CD38 also encodes several related cyclases. These include a second human gene, CD157 (BST-1), showing remarkable conservation of the exon structure as well as the structure of the encoded
Acta Haematologica – Karger
Published: Aug 1, 2001
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