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The availability of genetically engineered mice allows the unraveling of the role of specific proteins in mechanisms of ischemic brain injury.

The presence of macrophages in the Rag2−/− γc−/− mice allows the paracrine loop with tumor cells to take place and thus enhances invasiveness in response to EGF.

The lower toxicity of DMXAA in these knockout mice allows the use of higher drug doses, which restored both apoptosis induction and tumour blood flow inhibition responses.

Freeze-fracture immunolabeling of brain tissue from transgenic mice allows the clear identification of NG2 cells using anti-GFP antibodies; the results showed clusters of AMPA receptor-immunoreactive particles along the NG2 cell processes [ 30].

Disappearance of the mucus layer in MMP13+/+ mice allows the intestinal bacteria to interact with IECs and Paneth cells, resulting in increased local inflammation and activation of Paneth cells.

The ability to control transgene expression in mice allows the researcher to initiate tissue-specific changes at relevant time-points and, in the case of oncogenic transgenes such as PyV mT, mimic disease initiation (induction) and treatment (de-induction).

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The team developed a decoy drug that, in mice, allowed the animals to form new connections as adults.

Three scientists shared an award for developing a way to eliminate or "knock out" specific genes in mice, allowing the creation of animal models to study many human ailments.

To address these limitations, we examined complete isolated myofibres from mutant mice, allowing the ready scrutiny of all myonuclei and satellite cells (the resident stem cells of adult muscle [17]).

This statistical equivalency of mice allowed the use of a pseudo-randomization convenience allocation to assign mice to identified cages.

Fertility of single MuRF1 or MuRF2 KO mice allowed the generation of dKO strains by breeding them together.

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