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The abnormal swelling of Müller cells In Dp71-null mice involves the action of inflammatory mediators.

The induction of collagen-induced arthritis in susceptible mice involves the activation of helper T cells and B cells [39], [40].

Similarly, the control of mouse cytomegalovirus infection in certain strains of mice involves the recognition of peptide-MHC class I complexes through the activation of Ly49 receptors [40].

The creation of knockout mice involves the modification of the genome of mouse embryonic stem (ES) cells through a variety of processes including homologous recombination or other mutagenic procedures [1].

These results suggested that the enhanced synaptic trafficking of AMPAR in the adult mutant mice involves the activation of ADF/cofilin.

Embryonic development in mice involves the migration of primordial germ cells (GCs) to the genital ridge and their subsequent differentiation into gonocytes.

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Other genetic constructs in mice involving the genes p53, ptc1, and Nf1 have produced tumors remarkably similar to some of the human pediatric neoplasms.

While changes in Cu isotopes can clearly be related to the loss of metal binding to the protein, the change in Zn isotopes is only consistent with a genetic modification of the mice involving the PrP gene.

These data further support the conclusion that the changes in gene expression in the mutant mice involving the chromosome X can be explained by genetic background effects.

Endotoxin (ET -resistant mET -resistantC3H/HeJ mechanismsve the mutatinn of Toll-like reC3H/HeJ4 (TLR-4) by which ET signals to increase TNF-α production in micecytes.

Application of the data analysis pipeline outlined in Figure  1 revealed that the most thematically diverse alterations specific for C57BL/6.NOD- Aec1Aec2 mice, involving the most EM-related GSs and EM-associated GSs, occurred between 4 and 8 weeks of age.

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