Gandrillon O, Ferrand N, Michaille J J, Roze L, Zile M H, Samarut J
Laboratoire de Biologie Moléculaire et Cellulaire, CNRS UMR49, INRA, Ecole Normale Supérieure de Lyon, France.
Oncogene. 1994 Mar;9(3):749-58.
In AEV-transformed erythroleukemic cells the v-erbA gene product is likely to antagonize the function of triiodothyronine (T3) and retinoic acid (RA) receptors and thereby to block cell differentiation. We have thus investigated the effects of T3 and RA on normal early erythrocytic progenitor cells. Here we show: (1) that either RA or T3 play an essential role during the early commitment to erythrocytic differentiation, (2) that both T3 and RA induce death by apoptosis and a strong inhibition of self-renewal in progenitor cells grown in the absence of differentiation-inducing agents and (3) that the v-erbA oncogene renders erythrocytic progenitor cells insensitive to apoptosis and to self-renewal inhibition induced by RA or T3. The behaviour of a non-transforming mutant of v-erbA suggests that this v-erbA-induced protection is related to its transforming potential.
在禽成红细胞增多症病毒（AEV）转化的红白血病细胞中，v-erbA基因产物可能拮抗三碘甲状腺原氨酸（T3）和视黄酸（RA）受体的功能，从而阻断细胞分化。因此，我们研究了T3和RA对正常早期红细胞祖细胞的影响。我们在此表明：（1）RA或T3在早期红细胞分化的定向过程中发挥着重要作用；（2）T3和RA均可诱导细胞凋亡死亡，并强烈抑制在无分化诱导剂情况下培养的祖细胞的自我更新；（3）v-erbA癌基因使红细胞祖细胞对RA或T3诱导的细胞凋亡和自我更新抑制不敏感。v-erbA的一个非转化突变体的行为表明，这种v-erbA诱导的保护作用与其转化潜能有关。
