synaptophysin Search Results


synaptophysin  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc synaptophysin
Synaptophysin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nb300  (Novus Biologicals)
90
Novus Biologicals nb300
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synaptophysin  (Novus Biologicals)
93
Novus Biologicals synaptophysin
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Synaptophysin, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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icc 5461s mouse anti myosin heavy chain myhc  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc icc 5461s mouse anti myosin heavy chain myhc
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
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proteintech 17785 1 ap china psd95  (Proteintech)
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Proteintech proteintech 17785 1 ap china psd95
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
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synaptophysin  (R&D Systems)
93
R&D Systems synaptophysin
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Synaptophysin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti synaptophysin  (R&D Systems)
93
R&D Systems anti synaptophysin
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Anti Synaptophysin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti synaptophysin  (Novus Biologicals)
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FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Rabbit Anti Synaptophysin, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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paav1 hsyn dio mgfpsynaptophysin mruby  (Addgene inc)
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Addgene inc paav1 hsyn dio mgfpsynaptophysin mruby
FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Paav1 Hsyn Dio Mgfpsynaptophysin Mruby, supplied by Addgene inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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synaptophysin af647  (Novus Biologicals)
92
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FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, <t>synaptophysin,</t> and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).
Synaptophysin Af647, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, synaptophysin, and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).

Journal: The FASEB Journal

Article Title: Deficiency of IKKβ in neurons ameliorates Alzheimer's disease pathology in APP ‐ and tau‐transgenic mice

doi: 10.1096/fj.202201512r

Figure Lengend Snippet: FIGURE 5 Deficiency of IKKβ in neurons improves cognitive function and attenuates synaptic impairments in APP-transgenic mice. Six-month-old APP-transgenic (APPtg) and non-transgenic (APPwt) mice with (ko) and without (wt) deletion of neuronal IKKβ were examined for cognitive function with Morris water maze test. During the training phase, APPtgIKKβ-wt mice reached the escape platform with significantly longer traveling distance than APPwtIKKβ-wt littermate mice (A; two-way ANOVA followed by Bonferroni post-hoc test, n is shown in the figure). Deletion of IKKβ in neurons (APPtgIKKβ-ko) significantly reduced the traveling time and distance to the escape platform compared with APPtgIKKβ-wt mice (A, B; two-way ANOVA followed by Bonferroni post-hoc test). IKKβ deficiency affected the swimming speed neither of APPtg mice, nor for each mouse at different training time points (C; two-way ANOVA, p > .05). However, APPtgIKKβ-wt mice swam much faster than non-APP transgenic (APPwtIKKβ-wt) mice with unknown reasons (C; two-way ANOVA followed by Bonferroni post-hoc test). In the probe trial, APPtg and APPwt mice with and without IKKβ deficiency did not differ in the frequency, with which the mice visited the region where the platform was previously located (D; one-way ANOVA, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, and the amount of synaptic structure proteins, Munc18-1, SNAP25, synaptophysin, and PSD-95 in the brain homogenate of 6-month-old APPtg and APPwt mice (E–K). Transgenic expression of APP increases cleaved caspase-3, and neuronal deficiency of IKKβ recovers it (F; one-way ANOVA, n ≥ 7 per group). Deficiency of IKKβ in neurons was associated with a higher level of PSD-95 and Munc18-1 in APP-transgenic mice (H and I; one-way ANOVA followed by Bonferroni post-hoc test, n ≥ 5 per group).

Article Snippet: Proteins were then transferred onto polyvinylidene difluoride (PVDF) or nitrocellulose membranes and incubated overnight at 4°C with the following antibodies: mouse monoclonal antibody against Aβ (clone W0- 2; Sigma- Aldrich); rabbit monoclonal antibodies against beclin1 (clone D40C5), phosphor- glycogen synthase kinase (GSK)- 3β (clone D3A4), GSK- 3β (clone 27C10), phospho- CREB (Ser133) (clone 87G3), CREB (clone 48H2), cleaved Caspase- 3 (clone 5A1E), PSD- 95 (clone D27E11), synaptophysin (clone D8F6H), SNAP25 (clone D110), and Munc18- 1 (clone D4O6V), and rabbit polyclonal antibodies against LC3B (Cat.- No: NB100- 2220; Novus Biologicals, Centennial, USA), SQSTM1/p62 (Cat.- No: 5114), phospho- p38- MAPK (Thr180/Tyr182) (Cat.- No: 9211), p38- MAPK (Cat.- No: 9212), and protein phosphatase type 2A (PP2A) catalytic subunit (Cat.- No: 2038) (all antibodies except anti- LC3B were bought from Cell Signaling Technology, Danvers, USA).

Techniques: Transgenic Assay, Western Blot, Expressing

FIGURE 10 Deficiency of IKKβ in neurons does not affect cognitive function and even increases apoptosis in the brains of tau-transgenic mice. In the water maze test, 9-month-old TautgIKKβfl/flCre+/− (IKKβ ko) and TautgIKKβfl/flCre−/− (IKKβ wt) littermate mice did not differ in traveling latency and distance to reach the escape platform during the training phase (A and B; two-way ANOVA, p > .05, n ≥ 6 per group), nor in the frequency with which the mice visited the region where the platform was previously located during the probe trial (C; t test, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, phosphorylation level of CREB, and the amount of synaptic structure proteins, Munc18-1, SNAP25, synaptophysin, and PSD-95 in the brain homogenate of tau-transgenic mice (D–M). Deficiency of IKKβ in neurons does not alter the protein levels of various synaptic proteins (E–H; t test, p > .05, n ≥ 4 per group), nor the ratio of phosphorylated (p-) to total (t-) CREB (J and K; t test, p > .05, n ≥ 6 per group). Surprisingly, IKKβ deficiency significantly increases the protein level of cleaved caspase-3 in the brains of 9-month-old tau-transgenic mice (M; t test, n ≥ 9 per group).

Journal: The FASEB Journal

Article Title: Deficiency of IKKβ in neurons ameliorates Alzheimer's disease pathology in APP ‐ and tau‐transgenic mice

doi: 10.1096/fj.202201512r

Figure Lengend Snippet: FIGURE 10 Deficiency of IKKβ in neurons does not affect cognitive function and even increases apoptosis in the brains of tau-transgenic mice. In the water maze test, 9-month-old TautgIKKβfl/flCre+/− (IKKβ ko) and TautgIKKβfl/flCre−/− (IKKβ wt) littermate mice did not differ in traveling latency and distance to reach the escape platform during the training phase (A and B; two-way ANOVA, p > .05, n ≥ 6 per group), nor in the frequency with which the mice visited the region where the platform was previously located during the probe trial (C; t test, p > .05, n ≥ 6 per group). Western blotting was used to detect cleaved caspase-3, phosphorylation level of CREB, and the amount of synaptic structure proteins, Munc18-1, SNAP25, synaptophysin, and PSD-95 in the brain homogenate of tau-transgenic mice (D–M). Deficiency of IKKβ in neurons does not alter the protein levels of various synaptic proteins (E–H; t test, p > .05, n ≥ 4 per group), nor the ratio of phosphorylated (p-) to total (t-) CREB (J and K; t test, p > .05, n ≥ 6 per group). Surprisingly, IKKβ deficiency significantly increases the protein level of cleaved caspase-3 in the brains of 9-month-old tau-transgenic mice (M; t test, n ≥ 9 per group).

Article Snippet: Proteins were then transferred onto polyvinylidene difluoride (PVDF) or nitrocellulose membranes and incubated overnight at 4°C with the following antibodies: mouse monoclonal antibody against Aβ (clone W0- 2; Sigma- Aldrich); rabbit monoclonal antibodies against beclin1 (clone D40C5), phosphor- glycogen synthase kinase (GSK)- 3β (clone D3A4), GSK- 3β (clone 27C10), phospho- CREB (Ser133) (clone 87G3), CREB (clone 48H2), cleaved Caspase- 3 (clone 5A1E), PSD- 95 (clone D27E11), synaptophysin (clone D8F6H), SNAP25 (clone D110), and Munc18- 1 (clone D4O6V), and rabbit polyclonal antibodies against LC3B (Cat.- No: NB100- 2220; Novus Biologicals, Centennial, USA), SQSTM1/p62 (Cat.- No: 5114), phospho- p38- MAPK (Thr180/Tyr182) (Cat.- No: 9211), p38- MAPK (Cat.- No: 9212), and protein phosphatase type 2A (PP2A) catalytic subunit (Cat.- No: 2038) (all antibodies except anti- LC3B were bought from Cell Signaling Technology, Danvers, USA).

Techniques: Transgenic Assay, Western Blot, Phospho-proteomics