Disease relevance of Emid1

• Transgenic mice expressing the c-Myc oncogene driven by the immunoglobulin heavy chain enhancer (Emu) develop B-cell lymphoma and exhibit a mean survival time of approximately 6 months [1].
• Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice [2].
• The phenotype of tumors from IgH/c-myc YAC transgenic mice with or without Emu (B220+, IgM+/IgD+) is reminiscent of Burkitt's lymphoma [3].
• We have used provirus tagging in the Emu Bmi1 mice to identify genes that cooperate with Bmi1 in lymphomagenesis [4].
• We here discuss some circumstances in which lymphoid cell overexpression of a cell death antagonist, the Bcl2 protein, in E mu-bcl2 transgenic mice can contribute to the development of lymphomas and plasmacytomas [5].

High impact information on Emid1

• Transgenic mice bearing a c-myc oncogene subjugated to the lymphoid-specific immunoglobulin heavy chain enhancer (E mu) develop clonal B lymphoid malignancies, but most young E mu-myc mice lack malignant clones [6].
• To study the role of thymic medullary epithelium in tolerance induction, the third and fourth branchial clefts of embryos from E mu-Kb transgenic mice, which express the major histocompatibility complex class I antigen H-2Kb exclusively on medullary thymic epithelium, were grafted to athymic nude mice [7].
• B-cell tumorigenesis occurs in the translocus mice, even when the entire Emu intron enhancer region between the joining segments and switch mu is deleted [3].
• MoMLV infection in Emu Bmi1 transgenic mice accelerated lymphoma development [4].
• Pertubation of B and T cell development and predisposition to lymphomagenesis in Emu Bmi1 transgenic mice require the Bmi1 RING finger [4].

Biological context of Emid1

• The widespread, but individually distinct expression patterns of all Emu gene family members suggest multiple functions during mouse embryogenesis [8].
• Despite that Emu was reported to efficiently control the in vivo expression of other associated transgenes, it is not sufficient to sustain GFP expression in transgenic mice and to counteract developmental silencing programs that occur in the embryo [9].
• Effect of the Emu IgH enhancer on expression of a GFP reporter gene in transfected B cells and transgenic mice [9].

Anatomical context of Emid1

• After these tumours were rejected by alloantigen (H-2k/C3H background)-specific effector cells, the mice were challenged with the pre-B-lymphoma cell line derived from the original E mu/ret TGM (ret0-2) [10].

Analytical, diagnostic and therapeutic context of Emid1

• Oncogene-linked in situ immunotherapy of pre-B lymphoma arising in E mu/ret transgenic mice [10].

References