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© Research
Publication : Molecular immunology

Opposing Mcl-1, the GALIG proapoptotic gene is upregulated as neutrophils die and underexpressed in Acute Myeloid Leukemia cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Molecular immunology - 25 May 2013

Mollet L, Robinet P, Dubois M, Aurouet A, Normand T, Charpentier S, Sureau A, Grandclement C, Garnache-Ottou F, Deconinck E, Brulé F, Rohrlich PS, Legrand A

Link to Pubmed [PMID] – 23711389

Mol. Immunol. 2013 Nov;56(1-2):123-8

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.

http://www.ncbi.nlm.nih.gov/pubmed/23711389