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Results: 6

1.
Fig. 1.

Fig. 1. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

Nrf2-/- primary neuronal cultures are more vulnerable to 3NP. Nrf2-/- and Nrf2+/+ primary neuronal cultures were treated with 3NP. (A) LDH release was measured. (B) TUNEL staining was performed. **, P < 0.01 compared with WT mice.

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.
2.
Fig. 5.

Fig. 5. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

hPAP reporter is expressed in penumbra of malonate-induced lesions. Serial sections from malonate-lesioned ARE-hPAP reporter mice were stained with cresyl violet (A), hPAP histochemistry and nuclear fast red (B), and fluorescein-labeled GFAP (C).

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.
3.
Fig. 2.

Fig. 2. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

hPAP expression resulting from 3NP treatment in primary neurons. ARE-hPAP primary neuronal cultures were treated with 3NP. (A) LDH release and hPAP activation were measured. (B) hPAP activity was visualized by vector red, and GFAP was labeled with fluorescein.

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.
4.
Fig. 6.

Fig. 6. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

Ad-Nrf2-infected astrocyte transplants protect from malonate-induced lesions. hPAP+ astrocytes were infected with Ad-GFP or Ad-Nrf2-GFP. (A) GFP expression and hPAP histochemistry were visualized. Mice were lesioned 5 weeks posttransplant with malonate. Lesions were visualized by cresyl violet (B) and then were quantified (C). *, P < 0.05 compared with hemispheres receiving GFP-infected astrocytes.

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.
5.
Fig. 4.

Fig. 4. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

Nrf2-/- mice are more vulnerable to malonate in vivo. Malonate was administered to the right striatum with a contralateral saline control (n = 6 for Nrf2+/+; n = 8 for Nrf2+/-; n = 7 for Nrf2-/-). (A) Representative sections of mice with lesions are shown. (B) Average lesion size was quantified. Data are average ± SEM. *, P < 0.05 compared with WT mice.

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.
6.
Fig. 3.

Fig. 3. From: Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription.

Nrf2-/- mice are more vulnerable to 3NP in vivo. 3NP was administered (n = 6 for Nrf2+/+ and Nrf2+/-; n = 8 for Nrf2-/-). (A and B) Latency to fall on rotarod (A) and weight loss as a percentage of starting weight (B) were measured 4 h after the final injection. (C) Cresyl violet (Left) and Fluorojade-B (Right) were used to visualize lesions. (D) Average lesion volume was calculated on sections 200 μm apart. All data are average ± SEM. *, P < 0.05 compared with WT mice; **, P < 0.01 compared with WT and heterozygous mice.

Marcus J. Calkins, et al. Proc Natl Acad Sci U S A. 2005 January 4;102(1):244-249.

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