Figure 2
Figure 2. Study of novel pathogenic mechanisms of CLL in the TCL1-driven leukemia model. Overexpression (transgenic [tg]) or deficiency of different molecules in the Eμ-TCL1 transgenic mouse model variably affects the disease phenotype (BM, bone marrow; TAM, tumor-associated macrophages). The following mouse models have been crossed with Eμ-TCL1 mice: xid,91 pkcβ−/− (or pkcβ+/−),70 xbp1fl/flCD19-Cre,73 tir8−/−,72 dnrag1-tg,71 hs1−/−,79 rhoh−/−,59,80 p53−/−,75 id4−/−,76 miR29a/b-tg,35 fzd6−/−,89 cd44−/−,87 mif−/−,86 ROR1-tg,34 APRIL-tg,85 and baff-tg.84

Study of novel pathogenic mechanisms of CLL in the TCL1-driven leukemia model. Overexpression (transgenic [tg]) or deficiency of different molecules in the Eμ-TCL1 transgenic mouse model variably affects the disease phenotype (BM, bone marrow; TAM, tumor-associated macrophages). The following mouse models have been crossed with Eμ-TCL1 mice: xid,91 pkcβ−/− (or pkcβ+/−),70 xbp1fl/flCD19-Cre,73 tir8−/−,72 dnrag1-tg,71 hs1−/−,79 rhoh−/−,59,80 p53−/−,75 id4−/−,76 miR29a/b-tg,35 fzd6−/−,89 cd44−/−,87 mif−/−,86 ROR1-tg,34 APRIL-tg,85  and baff-tg.84 

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