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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and <t>BCL2</t> protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Image Search Results


Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and BCL2 protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Biochimica et biophysica acta. Molecular basis of disease

Article Title: Npc1 deficiency impairs microglia function via TREM2-mTOR signaling in Niemann-Pick disease type C.

doi: 10.1016/j.bbadis.2024.167478

Figure Lengend Snippet: Fig. 1. Loss of Npc1 impairs brain development in mouse. A Representative photograph of brain from Npc1−/−mice and littermate control at postnatal day 63 (P63). B Brain weight curves of Npc1−/−mice and littermate controls (n = 9; Page x genotype < 0.0001, Page < 0.0001, Pgenotype < 0.0001). C Representative coronal sections of Npc1−/−mice and littermate controls at P42 visualized by hematoxylin and eosin staining. D Quantification of the cortical thickness of mice from P1 to P63 (n = 3). E, F Representative confocal images and quantification of Filipin (white) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). G, H Representative confocal images and quantification of GFAP (red) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). I, J Repre sentative confocal images and quantification of MBP (green) and DAPI (blue) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). K, L Representative confocal images and quantification of cleaved-Caspase3 (c.CASP3, green) staining in the cortex of Npc1+/+ and Npc1−/−mice at P42 (n = 3). M Western blot analysis for c.CASP3, BAX and BCL2 protein expression in the brain of Npc1−/−mice and littermate controls (n = 3). Results are presented as Mean ± SEM. n.s., not sig nificant. *P < 0.05, **P < 0.01 and ***P < 0.001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The primary and secondary antibodies were used as follows: cleaved-Caspase3 (Cell Signaling Technology, USA; Cat No. 9664), BAX (Cell Signaling Technology, USA; Cat No. 14796), BCL2 (BOSTER, China; Cat No. BA0412), APOE (Abcam, UK; Cat No. ab183597), CTSD (Abcam, UK; Cat No. ab75852), Npc1 (Abcam, UK; Cat No. ab134113), Npc2 (Abcam, UK; Cat No. ab218192), TREM2 (Cell Signaling Technology, USA; Cat No. 76765), TREM2 (R&D Systems, USA; Cat No. AF1729), TREM2 (Abcam, UK; Cat No. ab305103), SYK (Cell Signaling Technology, USA; Cat No.13198), p-SYK (Cell Signaling Technology, USA; Cat No.2710), AKT (Cell Signaling Technology, USA; Cat No.4691), p-AKT (Cell Signaling Technology, USA; Cat No.13038), GSK3β (Cell Signaling Technology, USA; Cat No. 12456), p-GSK3β (Cell Signaling Technology, USA; Cat No. 5558), mTOR (Cell Signaling Technology, USA; Cat No. 2983), p-mTOR (Cell Signaling Technology, USA; Cat No. 5536), S6K1 (Cell Signaling Technology, USA; Cat No. 34475), p-S6K1 (Cell Signaling Technology, USA; Cat No. 9234), 4EBP1 (Cell Signaling Technology, USA; Cat No. 9644), p-4EBP1 (Cell Signaling Technology, USA; Cat No. 9451), CD63 (Abcam, UK; Cat No. ab217345), GFAP (Cell Signaling Technology, USA; Cat No. 80788), β-Actin (Affinity Biosciences, USA; Cat No. AF7018), β-Tubulin (Absin, China; Cat No. abs830032), Goat anti-Rabbit IgG-HRP (Absin, China; Cat No. abs20040), Goat anti-Mouse IgG-HRP (Absin, China; Cat No. abs20039), Rabbit anti-Sheep IgG-HRP (Abcam, UK; Cat No. ab6747).

Techniques: Control, Staining, Western Blot, Expressing