Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.

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* Figure A in S1 File Body weight (g) n=8/group
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Fig. 1. Loss of circadian rhythms in iKO mice.
Fig. 6. Transgenic expression of αLNNd and mag in dyW/dyW mice improves muscle function, increases body weight, and prolongs life span. Transgenic expression.
Fig. 2. Increased Aβ plaque load in 16-month-old APP/PS1;C3 KO mice.
Cognitive deficits in APPPS1‐21 mice.
Fig. 1. FMRP deficiency leads to increased NSC activation in the adult dentate gyrus. FMRP deficiency leads to increased NSC activation in the adult dentate.
Malat1 is a neuron‐enriched nuclear‐retained ncRNA that is localized to nuclear speckles. Malat1 is a neuron‐enriched nuclear‐retained ncRNA that is localized.
Fig. 5. Circulating PPi concentration does not correlate with severity of calcification phenotype in mice. Circulating PPi concentration does not correlate.
Fig. 3. Features of PH in KRasLA2 transgenic mice.
Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.
Fig. 2 Activity-dependent dynamics of β-actin mRNP in neurons from MCP×MBS mouse.(A and B) Examples of β-actin mRNP merge (A) and split (B) events. Activity-dependent.
Fig. 4. Bexarotene promotes PPARδ activation of target genes in mouse brain and muscle. Bexarotene promotes PPARδ activation of target genes in mouse brain.
Fig. 1. APP/PS1;C3 KO mice show improved cognitive flexibility (reversal) compared to APP/PS1 mice at 16 months of age. APP/PS1;C3 KO mice show improved.
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Dendritic spine density at P30 is elevated on isolated PirB−/− neurons in layer 2/3 after sparse excision of PirB at E15.5. Dendritic spine density at.
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Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Fig. 4 SDPS alters parvalbumin-positive interneuron properties and decreases inhibitory transmission in the hippocampus. SDPS alters parvalbumin-positive.
Fig. 4. MATE1 transcription in RCC.
Fig. 2 STED microscopy of isolated cardiomyocytes from mice treated with MP-rhodamine–loaded CaPs. STED microscopy of isolated cardiomyocytes from mice.
Fig. 4. Expression of HGF in liver ECs cooperates with NOX4 inhibition to enhance engraftment of regenerative hepatocytes. Expression of HGF in liver ECs.
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Fig. 1. mGlu7 expression is reduced in RTT autopsy samples.
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Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 7 Improvement of clinical score and axon pathology by nasal IL-4 treatment during chronic EAE. Improvement of clinical score and axon pathology by.
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Volume 16, Issue 6, Pages (August 2016)
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
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Fig. 6 Anticancer effects in PyMT-MMTV syngeneic and MDA-MB-231 xenograft-bearing mice. Anticancer effects in PyMT-MMTV syngeneic and MDA-MB-231 xenograft-bearing.
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Fig. 1. Specificity of FolamiR uptake in cancer cells in culture.
Fig. 7. Scale-up of AAV vector–mediated liver gene transfer of secretable GAA to nonhuman primates. Scale-up of AAV vector–mediated liver gene transfer.
Fig. 2. Thorase variants cause impaired GluA2 endocytosis and trafficking in mouse primary cortical neurons. Thorase variants cause impaired GluA2 endocytosis.
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Formation of papilloma lesions in the UroIICre+Fgfr3+/K644EK-RasG12D/+ model. Formation of papilloma lesions in theUroIICre+Fgfr3+/K644EK-RasG12D/+model.
Fig. 1 KCC2 down-regulation is prevented in sortilin-deficient mice.
The complexity and the total dendritic length of ApoE4 adult-born granule cells are significantly reduced. The complexity and the total dendritic length.
Fig. 2. Deficiency of neuronal HS leads to reduced neuroinflammation.
Fig. 3. Neuroprotective effects of silibinin against KA-induced excitotoxicity. (A) Silibinin was intraperitoneally injected for 8 days, starting 1 day.
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Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.
Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.
FKBP1b counters the age-related decrease in hippocampal MAP2 protein expression. FKBP1b counters the age-related decrease in hippocampal MAP2 protein expression.
At P23, dendritic spine density on L2/3 pyramidal cells in PirB−/− visual cortex is similar to that of PirB+/+. At P23, dendritic spine density on L2/3.
Fig. 4. Plaque-associated microglia and astrocytes and brain cytokines were altered in APP/PS1;C3 KO mice compared to APP/PS1 mice. Plaque-associated microglia.
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Fig. 3. HERV-K–induced neuronal toxicity in vivo.
Fig. 1. APP/PS1;C3 KO mice show improved cognitive flexibility (reversal) compared to APP/PS1 mice at 16 months of age. APP/PS1;C3 KO mice show improved.
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Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. (A) NeuN immunoreactivity in hippocampal CA3, CA1, and dentate gyrus (DG) and prefrontal cortex (PFC) regions in APP/PS1 and APP/PS1;C3 KO mice. Scale bars, 50 μm. (B) APP/PS1;C3 KO mice had more neurons in hippocampal CA3 compared to APP/PS1 mice (*P < 0.05, unpaired t test). (C to E) No significant differences were observed in neuron numbers in CA1, dentate gyrus, and PFC between APP/PS1 and APP/PS1;C3 KO mice. (F) Age-dependent neuron loss was observed between P30 and 16 months of age in WT and APP/PS1 mice and also between 4 and 16 months of age in APP/PS1 mice. However, neuron loss was not observed in C3 KO or APP/PS1;C3 KO mice (*P < 0.05, **P < 0.01, two-way ANOVA and Bonferroni post hoc test; n = 6 to 8; six equidistant planes, 150 μm apart). Qiaoqiao Shi et al., Sci Transl Med 2017;9:eaaf6295 Published by AAAS