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Papers In Press, published online ahead of print May 24, 2002
IGBMC, CNRS/INSERM/ULP, Illkirch 67404
Corresponding Author: cegly{at}igbmc.u-strasbg.fr
Mouse F9 embryocarcinoma (EC) cells constitute a well established cell-autonomous model system for investigating retinoic acid (RA) signaling in vitro. RA induces the differentiation of F9 cells grown as monolayers into endodermal-like cells and decreases their rate of proliferation. Knock-out of the retinoic X receptor alpha (RXRa) gene abolishes endodermal differentiation and the induction of several endogenous RA-responsive genes. RXRa null cells are also drastically impaired in their anti-proliferative response to RA. The role of the RXRa phosphorylation site located in the N-terminal A region (Ser22), has been investigated here by establishing cell lines reexpressing RXRa either WT or mutated at the phosphorylation site (RXRaS22A) in a RXRa-null background. We show that Ser22 is dispensible for RA-induced endodermal differentiation, but is crucial for the expression of several RA-responsive genes. Ser22 is also indispensible for the anti-proliferative effect of RA and necessary for the RA-induced down-regulation of p21CIP and p27KIP CKIs proteins which are known to be involved in the control of cell cycle progression.
J. Biol. Chem, 10.1074/jbc.M203623200
Submitted on April 15, 2002
Revised on May 24, 2002
Accepted on May 23, 2002
The phosphorylation site located in the A region of RXRa is required for the anti-proliferative effect of retinoic acid and the activation of RA-target genes in F9 cells
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