ddit3 null alleles stock Search Results


ddit3 null alleles stock# 005530  (Jackson Laboratory)
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Jackson Laboratory ddit3 null alleles stock# 005530
A. Longitudinal intraocular pressure (IOP) measurements from WT and <t>Ddit3/Jun</t> -/- eyes at 5, 9, 10.5, and 12 months of age. Both genotype groups had significantly elevated IOPs at 9M, 10.5M, and 12M compared to 5M ( P< 0.001, n≥ 60 for each comparison). At these timepoints, Ddit3/Jun -/- eyes did not have a statistically significant reduction in IOP compared to WT, although Ddit3/Jun -/- eyes had slightly higher IOPs at 9M of age compared to WT ( n≥ 60, * P= 0.004, Two-way ANOVA, Holm-Sidak’s post hoc ). B. Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from WT and Ddit3/Jun -/- mice and percentages of optic nerves with noe, moderate (mod) and sev glaucomatous damage in 12M WT and Ddit3/Jun -/- mice. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration ( n≥ 54, P= 0.049, Chi square test). C. Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12M WT and Ddit3/Jun -/- retinas with corresponding noe or sev optic nerves. Sev Ddit3/Jun -/- retinas had 77.0±3.1% improved RGC survival compared to WT controls. RBPMS+ cells/mm 2 ±SEM for WT and Ddit3/Jun -/- respectively: Noe: 2899.6±111.0, 2765.4±49.8; Sev: 226.7±20.8, 2151.5±83.0 ( n= 6, * P <0.001, Two-way ANOVA, Holm-Sidak post-hoc ). Scale bars, 50μm.
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A. Longitudinal intraocular pressure (IOP) measurements from WT and Ddit3/Jun -/- eyes at 5, 9, 10.5, and 12 months of age. Both genotype groups had significantly elevated IOPs at 9M, 10.5M, and 12M compared to 5M ( P< 0.001, n≥ 60 for each comparison). At these timepoints, Ddit3/Jun -/- eyes did not have a statistically significant reduction in IOP compared to WT, although Ddit3/Jun -/- eyes had slightly higher IOPs at 9M of age compared to WT ( n≥ 60, * P= 0.004, Two-way ANOVA, Holm-Sidak’s post hoc ). B. Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from WT and Ddit3/Jun -/- mice and percentages of optic nerves with noe, moderate (mod) and sev glaucomatous damage in 12M WT and Ddit3/Jun -/- mice. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration ( n≥ 54, P= 0.049, Chi square test). C. Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12M WT and Ddit3/Jun -/- retinas with corresponding noe or sev optic nerves. Sev Ddit3/Jun -/- retinas had 77.0±3.1% improved RGC survival compared to WT controls. RBPMS+ cells/mm 2 ±SEM for WT and Ddit3/Jun -/- respectively: Noe: 2899.6±111.0, 2765.4±49.8; Sev: 226.7±20.8, 2151.5±83.0 ( n= 6, * P <0.001, Two-way ANOVA, Holm-Sidak post-hoc ). Scale bars, 50μm.

Journal: bioRxiv

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1101/2024.09.27.614559

Figure Lengend Snippet: A. Longitudinal intraocular pressure (IOP) measurements from WT and Ddit3/Jun -/- eyes at 5, 9, 10.5, and 12 months of age. Both genotype groups had significantly elevated IOPs at 9M, 10.5M, and 12M compared to 5M ( P< 0.001, n≥ 60 for each comparison). At these timepoints, Ddit3/Jun -/- eyes did not have a statistically significant reduction in IOP compared to WT, although Ddit3/Jun -/- eyes had slightly higher IOPs at 9M of age compared to WT ( n≥ 60, * P= 0.004, Two-way ANOVA, Holm-Sidak’s post hoc ). B. Examples of optic nerve cross sections with no or early (noe) and severe (sev) glaucomatous damage from WT and Ddit3/Jun -/- mice and percentages of optic nerves with noe, moderate (mod) and sev glaucomatous damage in 12M WT and Ddit3/Jun -/- mice. Ddit3/Jun deletion did not afford protection to RGC axons and in fact slightly worsened axonal degeneration ( n≥ 54, P= 0.049, Chi square test). C. Representative retinal flat mounts immunoassayed for RBPMS and quantification of RBPMS+ cells from 12M WT and Ddit3/Jun -/- retinas with corresponding noe or sev optic nerves. Sev Ddit3/Jun -/- retinas had 77.0±3.1% improved RGC survival compared to WT controls. RBPMS+ cells/mm 2 ±SEM for WT and Ddit3/Jun -/- respectively: Noe: 2899.6±111.0, 2765.4±49.8; Sev: 226.7±20.8, 2151.5±83.0 ( n= 6, * P <0.001, Two-way ANOVA, Holm-Sidak post-hoc ). Scale bars, 50μm.

Article Snippet: Ddit3 null alleles ( ) (Jackson Laboratory, Stock# 005530), floxed alleles of Jun ( ) ( Jun fl ), and the Six3-cre transgene ( ) (Jackson Laboratory, Stock# 019755) were backcrossed >10 times to both the C57BL/6J genetic background (>99% C57BL/6J) and the DBA/2J background (>99% DBA/2J).

Techniques: Comparison

A. Representative pattern electroretinography (PERG) traces and amplitude quantification ( B ) from Gpnmb + , WT, Ddit3 -/- , Jun -/- , and Ddit3/Jun -/- mice at 5, 9, and 12M. Normotensive Gpnmb + mice did not have significant decline in PERG amplitude at 9M (n≥21, P>0.05), but had a slight but significant decline in PERG amplitude by 12M compared to 5M (n≥21, P=0.007), Ocular hypertensive mice of all genotype groups had significant PERG amplitude decline at 9M and 12M compared to 5M (n≥34, P<0.001, two-way ANOVA, Holm-Sidak’s post hoc). At 9M and 12M, each ocular hypertensive group’s PERG amplitude was significantly lower than normotensive Gpnmb + controls (n≥20, P<0.001). No increase in PERG amplitude was observed between WT and Ddit3 -/- , Jun -/- , or Ddit3/Jun -/- groups at any timepoint measured. Scale bar: Y: 5μV, X: 100ms. C. Quantification of full-field ERG a-wave and b-wave ( D ) amplitudes. By 12M, each ocular hypertensive group had a slight but significant decline of electroretinography (ERG) a and b-wave amplitudes compared to 5M (n≥34, P<0.001, two-way ANOVA, Holm-Sidak’s post hoc), but not nearly to the same extent as PERG amplitude decline ( A ). Percentage of PERG and ERG amplitude declines at 9 and 12M are listed for each group in . E. PERG amplitude quantifications from 12M WT and Ddit3/Jun -/- retinas with noe and sev optic nerve damage. Neither genotype nor optic nerve damage level influenced PERG amplitude (n≥6, P >0.05, two-way ANOVA). Of note, PERG amplitudes were significantly reduced compared with 12M Gpnmb + ( n =21, 7.2±0.6) regardless of genotype or level of axonal damage. PERG amplitude (μV)±SEM: WT noe: 2.0±0.4, Ddit3/Jun -/- noe: 1.8±0.2, WT sev: 2.3±0.3, Ddit3/Jun -/- sev: 1.9±0.2 ( n≥ 6, P< 0.001, one-way ANOVA, Holm-Sidak’s post hoc ). Scale bar: Y: 5μV, X: 100ms. F. High-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of average RGC soma size from WT and Ddit3/Jun -/- retinas with noe and sev glaucomatous damage. Both genotype groups had significant reductions in RGC soma size in sev glaucoma compared to respective noe controls (* P <0.001). While Ddit3/Jun -/- noe retinas had slightly smaller RGCs (* P =0.044), Ddit3/Jun deletion did not attenuate RGC soma shrinkage in sev retinas. Soma size (μm 2 )±SEM from WT and Ddit3/Jun -/- retinas, respectively: noe: 143.1±3.9, 131.7±2.9; sev: 87.6±2.5, 78.3±3.0 (n≥5, two-way ANOVA, Holm-Sidak’s post hoc ).

Journal: bioRxiv

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1101/2024.09.27.614559

Figure Lengend Snippet: A. Representative pattern electroretinography (PERG) traces and amplitude quantification ( B ) from Gpnmb + , WT, Ddit3 -/- , Jun -/- , and Ddit3/Jun -/- mice at 5, 9, and 12M. Normotensive Gpnmb + mice did not have significant decline in PERG amplitude at 9M (n≥21, P>0.05), but had a slight but significant decline in PERG amplitude by 12M compared to 5M (n≥21, P=0.007), Ocular hypertensive mice of all genotype groups had significant PERG amplitude decline at 9M and 12M compared to 5M (n≥34, P<0.001, two-way ANOVA, Holm-Sidak’s post hoc). At 9M and 12M, each ocular hypertensive group’s PERG amplitude was significantly lower than normotensive Gpnmb + controls (n≥20, P<0.001). No increase in PERG amplitude was observed between WT and Ddit3 -/- , Jun -/- , or Ddit3/Jun -/- groups at any timepoint measured. Scale bar: Y: 5μV, X: 100ms. C. Quantification of full-field ERG a-wave and b-wave ( D ) amplitudes. By 12M, each ocular hypertensive group had a slight but significant decline of electroretinography (ERG) a and b-wave amplitudes compared to 5M (n≥34, P<0.001, two-way ANOVA, Holm-Sidak’s post hoc), but not nearly to the same extent as PERG amplitude decline ( A ). Percentage of PERG and ERG amplitude declines at 9 and 12M are listed for each group in . E. PERG amplitude quantifications from 12M WT and Ddit3/Jun -/- retinas with noe and sev optic nerve damage. Neither genotype nor optic nerve damage level influenced PERG amplitude (n≥6, P >0.05, two-way ANOVA). Of note, PERG amplitudes were significantly reduced compared with 12M Gpnmb + ( n =21, 7.2±0.6) regardless of genotype or level of axonal damage. PERG amplitude (μV)±SEM: WT noe: 2.0±0.4, Ddit3/Jun -/- noe: 1.8±0.2, WT sev: 2.3±0.3, Ddit3/Jun -/- sev: 1.9±0.2 ( n≥ 6, P< 0.001, one-way ANOVA, Holm-Sidak’s post hoc ). Scale bar: Y: 5μV, X: 100ms. F. High-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of average RGC soma size from WT and Ddit3/Jun -/- retinas with noe and sev glaucomatous damage. Both genotype groups had significant reductions in RGC soma size in sev glaucoma compared to respective noe controls (* P <0.001). While Ddit3/Jun -/- noe retinas had slightly smaller RGCs (* P =0.044), Ddit3/Jun deletion did not attenuate RGC soma shrinkage in sev retinas. Soma size (μm 2 )±SEM from WT and Ddit3/Jun -/- retinas, respectively: noe: 143.1±3.9, 131.7±2.9; sev: 87.6±2.5, 78.3±3.0 (n≥5, two-way ANOVA, Holm-Sidak’s post hoc ).

Article Snippet: Ddit3 null alleles ( ) (Jackson Laboratory, Stock# 005530), floxed alleles of Jun ( ) ( Jun fl ), and the Six3-cre transgene ( ) (Jackson Laboratory, Stock# 019755) were backcrossed >10 times to both the C57BL/6J genetic background (>99% C57BL/6J) and the DBA/2J background (>99% DBA/2J).

Techniques:

A. Representative PERG traces and quantification of PERG amplitudes from WT, Ddit3/Jun -/- , and Mkk4/7 -/- retinas 14 days post-CONC or Sham procedures. WT and Ddit3/Jun -/- PERG amplitudes significantly declined 14 days post-CONC (by 52.6±5.7, * P <0.001 and 57.9±7.9µV, * P =0.002, respectively), while Mkk4/7 -/- PERG amplitudes did not significantly decline ( n≥ 17, two-way ANOVA, Holm-Sidak’s post-hoc .). Scale bar: Y: 5μV, X: 100ms. B. Representative high-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of RGC soma size from WT, Ddit3/Jun -/- and Mkk4/7 -/- retinas 14 days post-Sham or CONC procedures. After CONC, WT and Ddit3/Jun -/- RGC soma sizes were reduced to 78.4±0.8% (* P =0.001) and 65.5±4.6% (* P <0.001) the size of respective RGCs after Sham procedures. Mkk4/7 -/- RGC soma sizes did not change after CONC compared to Sham ( P =0.586). Mkk4/7 -/- RGCs were significantly larger compared to WT (* P =0.006) and Ddit3/Jun -/- (* P <0.001) RGCs after CONC, and Ddit3/Jun -/- RGCs were significantly smaller than WT post-CONC (* P =0.002). Soma size (μm 2 )±SEM from WT, Ddit3/Jun -/- , and Mkk4/7 -/- mice, respectively: Sham: 154.5±2.8, 137.0±7.3, 155.8±3.2; CONC: 121.2±1.1, 89.7±6.3, 147.5±7.8 ( n ≥7, two-way ANOVA, Holm-Sidak’s post hoc ).

Journal: bioRxiv

Article Title: MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury

doi: 10.1101/2024.09.27.614559

Figure Lengend Snippet: A. Representative PERG traces and quantification of PERG amplitudes from WT, Ddit3/Jun -/- , and Mkk4/7 -/- retinas 14 days post-CONC or Sham procedures. WT and Ddit3/Jun -/- PERG amplitudes significantly declined 14 days post-CONC (by 52.6±5.7, * P <0.001 and 57.9±7.9µV, * P =0.002, respectively), while Mkk4/7 -/- PERG amplitudes did not significantly decline ( n≥ 17, two-way ANOVA, Holm-Sidak’s post-hoc .). Scale bar: Y: 5μV, X: 100ms. B. Representative high-resolution images of retinal flat mounts immunoassayed for RBPMS (scale bar, 50μm) and quantification of RGC soma size from WT, Ddit3/Jun -/- and Mkk4/7 -/- retinas 14 days post-Sham or CONC procedures. After CONC, WT and Ddit3/Jun -/- RGC soma sizes were reduced to 78.4±0.8% (* P =0.001) and 65.5±4.6% (* P <0.001) the size of respective RGCs after Sham procedures. Mkk4/7 -/- RGC soma sizes did not change after CONC compared to Sham ( P =0.586). Mkk4/7 -/- RGCs were significantly larger compared to WT (* P =0.006) and Ddit3/Jun -/- (* P <0.001) RGCs after CONC, and Ddit3/Jun -/- RGCs were significantly smaller than WT post-CONC (* P =0.002). Soma size (μm 2 )±SEM from WT, Ddit3/Jun -/- , and Mkk4/7 -/- mice, respectively: Sham: 154.5±2.8, 137.0±7.3, 155.8±3.2; CONC: 121.2±1.1, 89.7±6.3, 147.5±7.8 ( n ≥7, two-way ANOVA, Holm-Sidak’s post hoc ).

Article Snippet: Ddit3 null alleles ( ) (Jackson Laboratory, Stock# 005530), floxed alleles of Jun ( ) ( Jun fl ), and the Six3-cre transgene ( ) (Jackson Laboratory, Stock# 019755) were backcrossed >10 times to both the C57BL/6J genetic background (>99% C57BL/6J) and the DBA/2J background (>99% DBA/2J).

Techniques: