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(B ) Antibody staining of w 1118 control and drep-2 ex13 mutant brains, using antibodies against the postsynaptic ACh receptor subunit Dα7 and presynaptic BrpN−Term.
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Our brains use it sparingly.
To assess whether the gene expression changes correlated with HTT-specific inclusions in the YAC128 and HdhQ150 mouse models we examined mutant HTT and ubiquitin distribution in mouse brain using immunohistochemistry (Fig. 4).
To more precisely characterize the effect of pros LoF at the cellular level, we generated null-mutant MARCM NB clones in the developing postembryonic brain using prosv17.
To further examine the interaction between mutant V145E leptin and leptin receptor, coimmunoprecipitation analysis was performed from brain using a leptin receptor antibody.
First, we generated and characterized conditional mutant mice exhibiting deletion of mTOR in neural progenitors and neurons in the developing brain using Nestin-cre and Nex-cre lines, respectively.
The ChIP experiments were performed using the extract isolated from dissected brat mutant brains that are enriched with type II neuroblasts.
By using a new method to dissociate living brain cells and analyze them by fluorescence-activated cell sorting (FACS), we showed that only GalC+ oligodendrocytes had elevated levels of ROS in mutant brains.
All mutant brains examined exhibited cortical lamination defects (Fig. 3A L).
By P15, the mutant brains were similar histologically to brains analyzed at P21 (Fig. 4N Q).
Sucla2 mutant placenta as well as mutant embryonic brain, heart and skeletal muscle showed varying degrees of mtDNA depletion and mutant brains exhibited elevated levels of MMA.
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