"Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4-, GCN2-, GCN2.KO4ex, or GCN2-KO) are viable, fertile and overtly indistinguishable from wild-type mice, with little if any mRNA expressed from the mutant locus. Homozygous GCN2-deficiency is associated with altered inflammatory responses and altered stress responses, including sensitivity to nutritional deficiencies and aberrant eating behavior. As GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) to reduce global translation and activate stress-related transcription factors (such as NF-kappaB) to alleviate cellular injury or alternatively induce apoptosis, these GCN2.KO4 mutant mice may be useful for such immunology, inflammatory, immunity cell biology, or neurobiology research."
"Homozygous mice are viable and fertile with normal immune system development and function. They exhibit no spontaneous autoimmune disorders. No gene product (mRNA or protein) from the targeted gene is detected in the epididymis. At embryonic day 10.5, endogenous protein is absent from all cells at the maternal-fetal interface when both parents are homozygous for the targeted gene. Allogeneic and syngeneic pregnancy outcomes are unaffected by this mutation. In contrast to wild-type, anti-proliferative treatments (CTLA4-Ig, IFNalpha, or CpG-ODN) do not suppress T cell expansion both in vivo and in vitro. In addition, homozygous dendritic cells isolated from lymph nodes draining (induced) tumor sites have no suppressor activity. These mice may be useful in studies of pregnancy and reproductive immunology (tryptophan degradation, T cell activation, clonal expansion) as well as autoimmune disease, tissue transplantation, fostering, acquired tolerance/T cell anergy, and immunosuppressive pathways. "