To circumvent this safeguard against oncogene-driven neoplasia, cancer cells with deregulated MYC frequently exhibit defects in apoptotic pathways.
At restrictive condition, the rna14-11 mutant cells exhibit defects in cell cycle progression with high level of septation.
Ozz−/− mutants exhibit defects in myofibrillogenesis and myofiber differentiation.
Consistent with this possibility we also show that elg1 mutants exhibit defects in cohesion.
Our results show that the dRecQ4 mutants exhibit defects in DNA replication.
Mice with Atg5−/− hematopoietic cells exhibit defects in T cell homeostasis [28].
Two strains of proprotein convertase KO mice, Furin and PACE4, exhibit defects in the vasculature and heart, while the other 8 proprotein convertase KO mice exhibit defects in hormone production, fertility, and lipid metabolism [71].
Vav null macrophages [25] exhibit defects in LPS-induced ERK and p38 MAPK signalling while JNK responses are normal [25].
Of the TGFβ isoform null mouse lines, only Tgfb2 mutant mice exhibit defects in kidney development [6], [12], [13], [14].
Finally, Type D blisters exhibit defects in vein patterning in addition to the formation of Type A-like blisters.
Mutants that inhibit cleavage at the NPTH site of HrcU homologs exhibit defects in the secretion of specific substrates.
