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Results: 13

1.
FIGURE 10.

FIGURE 10. From: Slc4a11 Gene Disruption in Mice.

Slit lamp examination of Slc4a11+/+ (A and B) and Slc4a11−/− (C and D) mice. Using diffuse illumination, both Slc4a11+/+ and Slc4a11−/− mice had normal appearing anterior segments without evidence of corneal opacification or edema (A and C). B and D, tangentially oriented slit beams confirm that a compact corneal architecture without edema exists in Slc4a11+/+ and Slc4a11−/− mice.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
2.
FIGURE 5.

FIGURE 5. From: Slc4a11 Gene Disruption in Mice.

NaBC1 immunofluorescence in vestibular endorgans of the Slc4a11+/+ and Slc4a11−/− mice. A and B, cross-section of the macula sacule. A, NaBC1 immunofluorescence was located in the stroma (ST) underneath the sacule sensory epithelia (SE) of Slc4a11+/+ mice. B, NaBC1 immunoreactivity was not detected in sensory epithelia or stroma of the macula sacule in Slc4a11−/− mice. DAPI (blue) shows cell nuclei. Bar in A and B, 100 μm.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
3.
FIGURE 9.

FIGURE 9. From: Slc4a11 Gene Disruption in Mice.

A, mean VsEP latencies for response peaks P1 and N1. B, mean P1-N1 amplitudes as a function of jerk amplitude. N1 latencies were significantly prolonged at all stimulus levels, and P1-N1 amplitudes were significantly smaller in the Slc4a11−/− mice. Moreover, the Slc4a11−/− mice demonstrated little if any increase in P1-N1 amplitude with increasing stimulus level, whereas the Slc4a11+/+ mice demonstrated normal amplitude intensity functions. Error bars, S.E.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
4.
FIGURE 6.

FIGURE 6. From: Slc4a11 Gene Disruption in Mice.

A, NaBC1 immunofluorescence in the spiral ligament (SL) (shown in red) simultaneously immunoreacted with antibodies against cochlin (shown in green) in the Slc4a11+/+ mouse. NaBC1 is exclusively located in the fibrocytes, whereas cochlin is seen in the extracellular matrix. NaBC1 expression was seen in fibrocytes of the spiral ligament. The stria vascularis (Stv) did not stain for NaBC1. B, higher magnification view in the Slc4a11+/+ mouse spiral ligament. NaBC1 immunoreactivity (in green) was present in the soma of fibrocytes (arrow). No immunoreactivity was seen in the nuclei (stained in blue). Bar, 25 μm (A) and 10 μm (B).

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
5.
FIGURE 3.

FIGURE 3. From: Slc4a11 Gene Disruption in Mice.

The vestibular endorgans from Slc4a11+/+ and Slc4a11−/− mice. Shown are the macula utricle (MU) and horizontal crista ampullaris (HCA) (A) posterior crista (B), and macula sacule (C) of the Slc4a11+/+ mouse. The arrows point to the normal appearance of the membranous labyrinth. D, in the Slc4a11−/− mouse, the membranous labyrinth was collapsed (arrows) over normal sensory epithelia (SE) of the macula utricle and horizontal crista ampullaris. E, collapse of the membranous labyrinth (arrows) in the posterior crista ampullaris. F, collapse of the membranous labyrinth (arrows) in the macula sacule. Bar, 100 μm (A and D) and 50 μm (B, C, E, and F).

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
6.
FIGURE 4.

FIGURE 4. From: Slc4a11 Gene Disruption in Mice.

NaBC1 immunofluorescence in Slc4a11+/+ and Slc4a11−/− mice. A, NaBC1 immunofluorescence in the spiral ligament (SL) of the cochlea from Slc4a11+/+ mice. A uniform NaBC1 pattern was observed from the base to apical portion of the cochlea. B, higher magnification view shows specific NaBC1 immunofluorescence in the spiral ligament and the spiral limbus (L). The organ of Corti (OC) is devoid of any immunofluorescence signal. C, NaBC1 immunofluorescence was not detected in the Slc4a11−/− mouse cochlea. D, high magnification view to corroborate the lack of NaBC1 immunofluorescence. Bar, 250 μm (A and C) and 25 μm (B and D).

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
7.
FIGURE 11.

FIGURE 11. From: Slc4a11 Gene Disruption in Mice.

A, corneal endothelium analysis in Slc4a11+/+ mice; B, corneal endothelium analysis in Slc4a11−/− mice. Corneal endothelium was stained with alizarin red to identify cell borders. No gross abnormalities were observed in endothelium from either group. Scale bar, 100 μm. Images of alizain red-stained central corneas were used to calculate central endothelial cell densities (C) and mean cell area (D). No significant differences in cell density or area were observed between Slc4a11+/+ and Slc4a11−/− mouse corneas.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
8.
FIGURE 7.

FIGURE 7. From: Slc4a11 Gene Disruption in Mice.

Superimposed ABR waveforms for Slc4a11+/+ (left) and Slc4a11−/− (right) mice (2 ABR replicates/animal). Each cluster of three (Slc4a11+/+) or two (Slc4a11−/−) superimposed displays is ordered in decreasing stimulus level intensity (75, 65, and 55 db). The vertical arrow in the upper left marks the 1 ms end of stimulus artifact and actual arrival of sound at the ear. Age groupings are as follows. A, young (Slc4a11+/+, 115–181 days; Slc4a11−/−, 151–175 days); B, middle (Slc4a11+/+, 204–211 days; Slc4a11−/−, 200–211 days); C, old (Slc4a11+/+, 398–464 days; Slc4a11−/−, 386–455 days).

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
9.
FIGURE 12.

FIGURE 12. From: Slc4a11 Gene Disruption in Mice.

Analysis of hematoxylin and eosin-stained cross-sections from Slc4a11+/+ and Slc4a11−/− mice corneas. A, cross-sections of the central cornea were examined for total thickness (t), epithelial thickness (e), and the height of the basal epithelial cell layer (b). Slc4a11+/+ (B) and Slc4a11−/− (C) corneal cross-sections have similar total corneal and epithelial thickness. Basal cell height was greater in Slc4a11−/− mice. Comparison of corneal architecture in Slc4a11+/+ and Slc4a11−/− mice. Total corneal thickness (D) and epithelial thickness (E) did not differ significantly between the two groups; however, basal cell height (F) and the ratio of basal cell height to epithelial thickness (G) were significantly greater (asterisks) in Slc4a11−/− mice than in Slc4a11+/+ mice. The stromal layer appeared normal in thickness but more disorganized.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
10.
FIGURE 13.

FIGURE 13. From: Slc4a11 Gene Disruption in Mice.

NaBC1 immunofluorescence in Slc4a11+/+ and Slc4a11−/− mouse cornea. A, NaBC1 immunofluorescence was present in layer 5 (endothelium), and less prominent but consistently observed immunofluorescence was seen in layer 1 epithelium. Much less evident was NaBC1 in the Bowman's (anterior membrane) layer 2. No staining was seen in layers 3 and 4. B, all cell nuclei stained with DAPI. C, merged image from A and B. D, NaBC1 immunofluorescence was not detected in any corneal layers of the Slc4a11−/− mice. E, cell nuclei stained with DAPI. F, merged image from D and E. Bar in A and D, 20 μm.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
11.
FIGURE 2.

FIGURE 2. From: Slc4a11 Gene Disruption in Mice.

The cochlea of the Slc4a11+/+ and Slc4a11−/− mice. A, low magnification view from the Slc4a11+/+ mouse cochlea. B, higher magnification view of the Slc4a11+/+ mouse cochlea. C, the normal spiral ganglia neurons (SGN) in Slc4a11+/+ mice. D, low magnification view from the Slc4a11−/− mouse cochlea. E, higher magnification of the Slc4a11−/− mouse cochlea. The inner (IHC) and outer hair cells (OHC) in the organ of Corti (OC) have a normal appearance. The stria vascularis (Stv), Reissner's (RM), and tectorial membrane (TM) were also normal. The spiral ligament (SL) showed a normal complement of fibrocytes. F, the spiral ganglia neurons of Slc4a11−/− mice. A and D were taken from similar cochlear regions (midbase). Bar, 100 μm (A and D), 50 μm (B and E), and 25 μm (C and F).

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
12.
FIGURE 1.

FIGURE 1. From: Slc4a11 Gene Disruption in Mice.

Insertional deletion of Slc4a11. A, restriction map of the retroviral gene trap vector, VICTR48. B, structural arrangement of 129 Sv/Evbrd mouse gene Slc4a11; diagram of the mutated Slc4a11 allele after insertion. C, immunoblot analysis of protein samples prepared from HEK293 cells transfected with wild-type NaBC1, cochlea, and cornea of wild-type (Slc4a11+/+), and knock-out (Slc4a11−/) mice using the C-terminal antibody to CL-NaBC1. D, HEK293 cells transfected with wild-type NaBC1, showing NaBC1 immunoreactivity. E, mock-transfected HEK293 cells showing lack of NaBC1 staining; F, Nomarski image of the same field in E. G, HEK293 cells transfected with wild-type NaBC1 were not stained when the Cl-NaBC1 antibody was preincubated with the immunizing peptide. H, Nomarski image of the same field in G. LTR, long terminal repeat.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.
13.
FIGURE 8.

FIGURE 8. From: Slc4a11 Gene Disruption in Mice.

Examples of VsEP waveforms for a typical Slc4a11+/+ mouse (left) and a representative Slc4a11−/− mouse (right). Stimuli were calibrated in jerk levels (change in acceleration over time, da/dt) and were defined in terms of db reference 1.0 g/ms, where 0 db produced a linear acceleration pulse with jerk amplitude of 1 g/ms (g = 9.8 m/s2). Stimulus amplitudes ranged from +6 db to −18 db. At +6 db, VsEPs were also collected with a forward masker (+6 M group), as described under “Experimental Procedures.” Each stimulus level shows two response waveforms to demonstrate response replication. As stimulus intensity is reduced, peak-to-peak amplitudes decrease and latencies increase until no response is visible at levels below threshold. VsEP thresholds for these two animals were scored at −13.5 and −10.5 db for Slc4a11+/+ and Slc4a11−/− mice, respectively.

Ivan A. Lopez, et al. J Biol Chem. 2009 September 25;284(39):26882-26896.

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