creb antibody (lb9) Search Results


creb  (Novus Biologicals)
93
Novus Biologicals creb
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 <t>cleaved</t> <t>caspase-3,</t> phosphorylation level of <t>CREB,</t> 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).
Creb, 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
https://www.bioz.com/result/creb/product/Novus Biologicals
Average 93 stars, based on 1 article reviews
creb - by Bioz Stars, 2026-05
93/100 stars
  Buy from Supplier
anti phospho creb s121  (Novus Biologicals)
92
Novus Biologicals anti phospho creb s121
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 <t>cleaved</t> <t>caspase-3,</t> phosphorylation level of <t>CREB,</t> 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).
Anti Phospho Creb S121, 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
https://www.bioz.com/result/anti phospho creb s121/product/Novus Biologicals
Average 92 stars, based on 1 article reviews
anti phospho creb s121 - by Bioz Stars, 2026-05
92/100 stars
  Buy from Supplier
creb monoclonal antibody lb 9  (Thermo Fisher)
N/A
CREB Monoclonal Antibody for Western Blot IF ICC IHC ELISA
   Buy from Supplier

Image Search Results


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