التفاصيل البيبلوغرافية
| العنوان: |
Immune development in mice fed diets complete in amino acids or lacking the essential amino acid (EAA) leucine is regulated by the eIF2 kinase GCN2. |
| المؤلفون: |
Aldrich, Carla J., Cundiff, Judy K., Beane, Joal D., Aakhus, Erin O., Yongjun Heo, Venard, Jacob M., McDaniel, Brent J., Bunpo, Piyawan, Seetharamaiah, G. S., McGrath, Barbara, Cavener, Douglas R., Anthony, Tracy G. |
| المصدر: |
FASEB Journal; Apr2007, Vol. 21 Issue 5, pA63-A63, 1/5p |
| مصطلحات موضوعية: |
PROTEIN synthesis, MESSENGER RNA, AMINO acids, LYMPHOCYTES, PHOSPHORYLATION, LABORATORY mice |
| مستخلص: |
Dietary deprivation of EAA results in reduced mRNA translation and repression of global protein synthesis. In liver, this is regulated in part by GCN2 phosphorylation of eukaryotic initiation factor-2 (eIF2α). To determine the role(s) of GCN2 in lymphocyte development and function, we examined the effect of 6 days of feeding diets devoid of the EAA leucine (-Leu) on immune cells of C57BL/6J (B6) mice or mice genetically lacking Gcn2 (Gcn2-/-). Gcn2-/- mice exhibit altered basal immune cell populations as compared to B6 mice. Gcn2-/- mice have decreased CD4+8+ thymocytes; increased % B220+, CD117+ and sIgM+ bone marrow cells, and decreased plasma IgG and IgM levels. Gcn2-/- mice also are more sensitive to EAA deficient diets. Feeding -- Leu diet to Gcn2-/- mice further reduced CD4+8+ thymocytes, CD19+ spleen cells, and decreased % B220+ bone marrow cells. Preliminary data suggest that the inability of thymus and spleen of Gcn2-/- mice to up-regulate eIF2α phosphorylation may be responsible for the decreased ability of Gcn2-/- cells to respond appropriately to EAA deficiency. Thus, we hypothesize that GCN2 plays an important role in development and function of immune cells in response to EAA deprivation. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
