Sentence examples for mouse fibroblasts lacking from inspiring English sources

Mouse fibroblasts lacking DNMT1 have been established in a p53-null background [30]; their chromocenters are undermethylated to varying levels in the cell population and, in many cells, the hypomethylation is sufficient to prevent recruitment of methyl-binding proteins.

Recycling of clathrin is essential for endocytosis, as mouse fibroblasts lacking GAK have severely impaired endocytosis (Lee et al. 2008).

Mouse fibroblasts lacking IGF1R cannot be transformed by known oncogenes, such as SV40 T antigen, papillomavirus E5 and overexpression of Ras (Sell et al, 1993).

IFNγ-induced mouse fibroblasts lacking the autophagic regulatory protein, Atg5, do not control avirulent T. gondii replication efficiently (Könen-Waisman and Howard, 2007) and Irga6 fails to load the PV in Atg5-deficient macrophages, forming cytosolic aggregates (Zhao et al., 2008).

IFNγ-induced mouse fibroblasts lacking the autophagic regulator, Atg5, restrict growth of avirulent ME49 strain of T. gondii weakly (Könen-Waisman and Howard, 2007), and Atg5-deficient macrophages stimulated with IFNγ and LPS are deficient in accumulating Irga6 at the PVM of the type II avirulent PTG strain of T. gondii (Zhao et al., 2008).

In contrast, mice deficient for Suv420h2 are viable [11], although mouse embryonic fibroblasts lacking this enzyme exhibit defects in telomere maintenance, which is consistent with the accumulation of H4K20me3 in telomeric heterochromatin [18].

An shRNA expression vector containing Msh2 target sequences was designed and used to transfect mouse embryonic fibroblasts lacking either alkylpurine DNA N-glycosylase (Mpg) or endonuclease III homologue (Nth1).

In mouse embryonic fibroblasts lacking the Suv39h histone methyltransferases there is no accumulation of HP1 proteins in heterochromatin.

Mouse embyronic fibroblasts lacking Zbtb7 were completely refractory to oncogene-mediated cellular transformation.

Finally, mouse embryonic fibroblasts lacking a functional Wrn helicase inhibited the immortalization of Safb1-null cells.

Similarly, mouse embryonic fibroblasts lacking MyD88 retained the ability to induce IFNα/β mRNA expression in response to viruses [ 33].