Centre de Biophysique Moléculaire, CNRS UPR 4301, affiliated with the Université d'Orléans-Pôle Universitaire Centre Val de Loire, Orléans, France.
Mol Immunol. 2013 Nov;56(1-2):123-8. doi: 10.1016/j.molimm.2013.04.012. Epub 2013 May 25.
GALIG gene expression induces apoptosis in cultured cells through a pathway still under investigation. It is highly expressed in leukocytes but weakly detectable in bone marrow, suggesting a role in the myeloid lineage homeostasis. We show here that GALIG-induced cell death is counteracted by the overexpression of MCL-1, a pro-survival member of the Bcl2 family. Moreover, during spontaneous neutrophil apoptosis, a substantial increase in GALIG gene expression is observed: GALIG still opposes MCL-1. Finally, in bone marrow and peripheral blood cells from patients with Acute Myeloid Leukemia type 2, the level of GALIG transcripts is massively down-regulated when compared to their normal counterparts, while MCL-1 is expressed to the same extent. These data suggest that GALIG could be a key player in the cell death pathway involved in leukocytes homeostasis and myeloid malignancies.
GALIG 基因表达通过一条仍在研究中的途径诱导培养细胞凋亡。它在白细胞中高度表达，但在骨髓中检测到的表达较弱，提示其在髓系细胞稳态中发挥作用。我们在这里表明，GALIG 诱导的细胞死亡可被抗凋亡 Bcl-2 家族成员 MCL-1 的过表达所拮抗。此外，在自发的中性粒细胞凋亡过程中，观察到 GALIG 基因表达的大量增加：GALIG 仍然对抗 MCL-1。最后，在急性髓系白血病 2 型患者的骨髓和外周血细胞中，与正常对照相比，GALIG 转录本的水平大量下调，而 MCL-1 的表达程度相同。这些数据表明，GALIG 可能是参与白细胞稳态和髓系恶性肿瘤的细胞死亡途径的关键因素。
