α7nachr Search Results


94
MedChemExpress agonist
Agonist, supplied by MedChemExpress, 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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SinaClon BioScience primers sequences for α7nachr and other genes
The sequence of primers for alpha7 <t> nicotinic acetylcholine receptor </t> <t> (α7nAChR), </t> caspase-3, cyclin B1, and GAPDH genes
Primers Sequences For α7nachr And Other Genes, supplied by SinaClon BioScience, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Millar Inc α7nachr
The sequence of primers for alpha7 <t> nicotinic acetylcholine receptor </t> <t> (α7nAChR), </t> caspase-3, cyclin B1, and GAPDH genes
α7nachr, supplied by Millar Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/native+%CE%B17+nachr/pmc02720620-330-36-22
Average 90 stars, based on 1 article reviews
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KU Leuven rag-1 knockout mice
The sequence of primers for alpha7 <t> nicotinic acetylcholine receptor </t> <t> (α7nAChR), </t> caspase-3, cyclin B1, and GAPDH genes
Rag 1 Knockout Mice, supplied by KU Leuven, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/rag1+%CE%B17nachr+double+knockout+mice/pmc05072409-91-10-52
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90
TriLink human α7 nachr mrna
The sequence of primers for alpha7 <t> nicotinic acetylcholine receptor </t> <t> (α7nAChR), </t> caspase-3, cyclin B1, and GAPDH genes
Human α7 Nachr Mrna, supplied by TriLink, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/human+%CE%B17+nachr+mrna/us09434724-1361-0-7
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Baier labs α7 nachr
Experimental design for pharmacological and molecular genetic manipulations
α7 Nachr, supplied by Baier labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/%CE%B17+nachr/pmc05979617-393-8-20
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GeneTex primary antibody α7nachr
The protein expression of <t>α7nAChR</t> (n=10 in each group). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.
Primary Antibody α7nachr, supplied by GeneTex, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/rabbit+anti+%CE%B17nachr+polyclonal+antibody/pmc11570470-102-21-24
Average 90 stars, based on 1 article reviews
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GenScript corporation rpab against α7 nachr antibody
A-B: Immunehistochemical analysis of vimentin (A) and <t>α7</t> <t>nAChR</t> (B) expression in mouse brain cortex. Images (A and B) photographed at 200X magnification C: Western blotting analysis of vimentin, α7 nAChR, phospho-IKKα/β and P65 expression levels in mouse vascular endothelial cells.
Rpab Against α7 Nachr Antibody, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/rabbit+anti+%CE%B17+nachr+ab/pmc05033352-91-85-90
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Shanghai GenePharma short interfering (si) rna specific for human α7-nachr
A-B: Immunehistochemical analysis of vimentin (A) and <t>α7</t> <t>nAChR</t> (B) expression in mouse brain cortex. Images (A and B) photographed at 200X magnification C: Western blotting analysis of vimentin, α7 nAChR, phospho-IKKα/β and P65 expression levels in mouse vascular endothelial cells.
Short Interfering (Si) Rna Specific For Human α7 Nachr, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/short+interfering++si++rna+specific+for+human+%CE%B17+nachr/pmc06671559-30-7-12
Average 90 stars, based on 1 article reviews
short interfering (si) rna specific for human α7-nachr - by Bioz Stars, 2026-10
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GeneTex anti-α7 nachr rabbit polyclonal antibody gtx10096
Expression levels of <t>α7</t> <t>nAChR</t> and Aβ in the brains of patients with AD and normal brains. (A) Images of the immunofluorescence double staining in the control and AD groups. (B) Aβ is expressed in the cytoplasm and extracellular matrix of cells. It was also found highly expressed in the brain slices of patients with AD, whereas the expression levels were minimal in healthy control brain sections following immunofluorescence double staining. (C) α7 nAChR was found expressed in the cytoplasm and reduced expression levels were observed in brain sections of patients with AD compared with healthy human brain sections, following immunofluorescence double staining. The cell nuclei are stained in blue using DAPI. Aβ-positive neurons are indicated in red and α3 nAChR-positive neurons are green. Scale bar, 20 µm. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control group. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease; IOD, integrated optical density.
Anti α7 Nachr Rabbit Polyclonal Antibody Gtx10096, supplied by GeneTex, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Babco Inc anti-α7 nachr antibody
Nicotine activation of ERK2 in hippocampal slices is mediated by <t>α7</t> nAChRs. a, Quantitative immunoblot demonstrates that 500 μm nicotine stimulated ERK2 MAPK activity, which is antagonized by 1 μm MLA in hippocampal slices from mice heterozygous for the L250T α7 <t>nAChR</t> transgene. Basal, 1.00 ± 0.22; nicotine (nic), 2.33 ± 0.13; MLA + nicotine, 1.34 ± 0.14. *Significant difference from basal level; p < 0.01, post hocTukey multiple comparison test. Representative immunoblot results are depicted below the response histogram. ERK1 (topband) activation paralleled that of ERK2; however, absolute levels of phospho-ERK1 were far below ERK2 and were not quantified. Slices from wild-type animals did not exhibit significant ERK2 MAPK activation with nicotine treatment, likely because of the rapid desensitization kinetics of wild-type α7 nAChRs precluding biochemical detection of ERK2 MAPK activation (Seguela et al., 1995). b, Quantitative immunoblot demonstrates that ERK2 MAPK activation by nicotine in cultured rat hippocampal slices is blocked by 1 μm MLA. Basal, 1.01 ± 0.08; nicotine, 1.66 ± 0.13; MLA + nicotine, 1.22 ± 0.09. *Denotes nicotine stimulation is significantly different from basal level;p < 0.001, post hoc Tukey multiple comparison test. Representative immunoblot results are depictedbelow the response histogram.
Anti α7 Nachr Antibody, supplied by Babco Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/anti+%CE%B17+nachr+antibody/pmc06762764-61-0-6
Average 90 stars, based on 1 article reviews
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90
NanoCarrier Co α7-nachr targeted nanocarrier
Nicotine activation of ERK2 in hippocampal slices is mediated by <t>α7</t> nAChRs. a, Quantitative immunoblot demonstrates that 500 μm nicotine stimulated ERK2 MAPK activity, which is antagonized by 1 μm MLA in hippocampal slices from mice heterozygous for the L250T α7 <t>nAChR</t> transgene. Basal, 1.00 ± 0.22; nicotine (nic), 2.33 ± 0.13; MLA + nicotine, 1.34 ± 0.14. *Significant difference from basal level; p < 0.01, post hocTukey multiple comparison test. Representative immunoblot results are depicted below the response histogram. ERK1 (topband) activation paralleled that of ERK2; however, absolute levels of phospho-ERK1 were far below ERK2 and were not quantified. Slices from wild-type animals did not exhibit significant ERK2 MAPK activation with nicotine treatment, likely because of the rapid desensitization kinetics of wild-type α7 nAChRs precluding biochemical detection of ERK2 MAPK activation (Seguela et al., 1995). b, Quantitative immunoblot demonstrates that ERK2 MAPK activation by nicotine in cultured rat hippocampal slices is blocked by 1 μm MLA. Basal, 1.01 ± 0.08; nicotine, 1.66 ± 0.13; MLA + nicotine, 1.22 ± 0.09. *Denotes nicotine stimulation is significantly different from basal level;p < 0.001, post hoc Tukey multiple comparison test. Representative immunoblot results are depictedbelow the response histogram.
α7 Nachr Targeted Nanocarrier, supplied by NanoCarrier Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B17nachr/%CE%B17+nachr+targeted+nanocarrier/pmc06058686-198-13-15
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Image Search Results


The sequence of primers for alpha7  nicotinic acetylcholine receptor   (α7nAChR),  caspase-3, cyclin B1, and GAPDH genes

Journal: Advanced Pharmaceutical Bulletin

Article Title: Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells

doi: 10.15171/apb.2020.008

Figure Lengend Snippet: The sequence of primers for alpha7 nicotinic acetylcholine receptor (α7nAChR), caspase-3, cyclin B1, and GAPDH genes

Article Snippet: The primers sequences for α7nAChR and other genes were obtained from Sinaclon (Tehran, Iran) and listed in .

Techniques: Sequencing

Experimental design for pharmacological and molecular genetic manipulations

Journal: British Journal of Pharmacology

Article Title: Hippocampal α7 nicotinic ACh receptors contribute to modulation of depression‐like behaviour in C57BL/6J mice

doi: 10.1111/bph.13769

Figure Lengend Snippet: Experimental design for pharmacological and molecular genetic manipulations

Article Snippet: Prenatal stress, which can induce depression‐like phenotypes, decreases α7 nAChR expression, with some of the strongest effects observed in DG (Baier et al. , 2015 ).

Techniques: Saline, Knockdown, shRNA, Suspension

Effect of α7 nAChR knockdown on behaviour in tests of depression‐like phenotypes. Time spent immobile in (A) the tail suspension and (B) forced swim tests following α7 nAChR knockdown in the hippocampus of C57BL/6J male mice. In the forced swim test, data are split into 5‐ and 10‐min time bins and represent the same assay; 10 animals were used per treatment group in the final analyses. Data are expressed as means ± SEM, and dots represent individual data points. Inset represents an example of viral infection (GFP‐positive cells in the dorsal hippocampus/DG). *P < 0.05, significantly different as indicated; ANOVA and partial least squares differences post hoc tests, for each time point.

Journal: British Journal of Pharmacology

Article Title: Hippocampal α7 nicotinic ACh receptors contribute to modulation of depression‐like behaviour in C57BL/6J mice

doi: 10.1111/bph.13769

Figure Lengend Snippet: Effect of α7 nAChR knockdown on behaviour in tests of depression‐like phenotypes. Time spent immobile in (A) the tail suspension and (B) forced swim tests following α7 nAChR knockdown in the hippocampus of C57BL/6J male mice. In the forced swim test, data are split into 5‐ and 10‐min time bins and represent the same assay; 10 animals were used per treatment group in the final analyses. Data are expressed as means ± SEM, and dots represent individual data points. Inset represents an example of viral infection (GFP‐positive cells in the dorsal hippocampus/DG). *P < 0.05, significantly different as indicated; ANOVA and partial least squares differences post hoc tests, for each time point.

Article Snippet: Prenatal stress, which can induce depression‐like phenotypes, decreases α7 nAChR expression, with some of the strongest effects observed in DG (Baier et al. , 2015 ).

Techniques: Knockdown, Suspension, Infection

The protein expression of α7nAChR (n=10 in each group). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Journal: IBRO Neuroscience Reports

Article Title: Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord

doi: 10.1016/j.ibneur.2024.10.002

Figure Lengend Snippet: The protein expression of α7nAChR (n=10 in each group). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Article Snippet: The filter membranes were blocked with 5 % nonfat milk for 1 h at room temperature and incubated with the primary antibody α7nAChR (1:1000, Genetex, USA), anti-BDNF (1:1000, Genetex, USA), anti-trkB (1:1000, Genetex, USA) and anti-KCC (1:1000, Genetex, USA) for overnight at 4°C.

Techniques: Expressing

Schematic diagram of the fluorescence of α7nAChR in the spinal cord (n=10 in each group). Scale bars are 50 μm.

Journal: IBRO Neuroscience Reports

Article Title: Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord

doi: 10.1016/j.ibneur.2024.10.002

Figure Lengend Snippet: Schematic diagram of the fluorescence of α7nAChR in the spinal cord (n=10 in each group). Scale bars are 50 μm.

Article Snippet: The filter membranes were blocked with 5 % nonfat milk for 1 h at room temperature and incubated with the primary antibody α7nAChR (1:1000, Genetex, USA), anti-BDNF (1:1000, Genetex, USA), anti-trkB (1:1000, Genetex, USA) and anti-KCC (1:1000, Genetex, USA) for overnight at 4°C.

Techniques: Fluorescence

A-B: Immunehistochemical analysis of vimentin (A) and α7 nAChR (B) expression in mouse brain cortex. Images (A and B) photographed at 200X magnification C: Western blotting analysis of vimentin, α7 nAChR, phospho-IKKα/β and P65 expression levels in mouse vascular endothelial cells.

Journal: PLoS ONE

Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier

doi: 10.1371/journal.pone.0162641

Figure Lengend Snippet: A-B: Immunehistochemical analysis of vimentin (A) and α7 nAChR (B) expression in mouse brain cortex. Images (A and B) photographed at 200X magnification C: Western blotting analysis of vimentin, α7 nAChR, phospho-IKKα/β and P65 expression levels in mouse vascular endothelial cells.

Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a RPAb against α7 nAChR from Genescript (Piscataway, NJ) and a rat anti-mouse Ly-6G (Gr-1) antibody from eBiosciences (San Diego, CA).

Techniques: Expressing, Western Blot

Elevation of intracellular calcium flux in HBMEC stimulated with E44 or ZD1 strains. HBMEC transfected with siRNAs of a scrambled sequence (CON), vimentin (Vim KD) and α7 nAChR (A7 KD) were loaded with Fura-2 AM as described in Methods and Materials. The monolayer was monitored for intracellular calcium flux for 10 minutes with 4 s intervals under an automated fluorescent microscope. Monolayer cells were stimulated with E44 or ZD (10 8 CFU) at the 120 s time point. The intensity of fluorescence at 340 nm and 380 nm was measured. The ratios of intensity of fluorescence at 340 nm and 380 nm were calculated for each time interval and depicted as continuous lines in (A–C). (G) The y axis represents the ratio, and x axis represents time (s). The 340 nm/380 nm ratio changes in each treatment were calculated and subjected to statistical analysis. WT HBMEC without any pre-treatment served as a control and are defined as one-fold (1.0). (*P<0.05; **P<0.01).

Journal: PLoS ONE

Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier

doi: 10.1371/journal.pone.0162641

Figure Lengend Snippet: Elevation of intracellular calcium flux in HBMEC stimulated with E44 or ZD1 strains. HBMEC transfected with siRNAs of a scrambled sequence (CON), vimentin (Vim KD) and α7 nAChR (A7 KD) were loaded with Fura-2 AM as described in Methods and Materials. The monolayer was monitored for intracellular calcium flux for 10 minutes with 4 s intervals under an automated fluorescent microscope. Monolayer cells were stimulated with E44 or ZD (10 8 CFU) at the 120 s time point. The intensity of fluorescence at 340 nm and 380 nm was measured. The ratios of intensity of fluorescence at 340 nm and 380 nm were calculated for each time interval and depicted as continuous lines in (A–C). (G) The y axis represents the ratio, and x axis represents time (s). The 340 nm/380 nm ratio changes in each treatment were calculated and subjected to statistical analysis. WT HBMEC without any pre-treatment served as a control and are defined as one-fold (1.0). (*P<0.05; **P<0.01).

Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a RPAb against α7 nAChR from Genescript (Piscataway, NJ) and a rat anti-mouse Ly-6G (Gr-1) antibody from eBiosciences (San Diego, CA).

Techniques: Transfection, Sequencing, Microscopy, Fluorescence, Control

E . coli K1 infection triggers IbeA-dependent activation of the vimentin signaling pathway at the host cell membrane. IbeA binds to its receptor Vim and co-receptor PSF that interact with α7n nAChR through lipid rafts. These communications trigger phosphorylation of signaling proteins (e.g., Vim, TAK1), which in turn activates the nuclear factor-kappaB (NF-κB) pathways via activation of the IκB kinase (IKK) complex. NF-κB activation resulted to the nuclear translocation of NF-κB, which induces the production of cytokines, chemokines, and others proinflammatory molecules in response to bacterial stimuli.

Journal: PLoS ONE

Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier

doi: 10.1371/journal.pone.0162641

Figure Lengend Snippet: E . coli K1 infection triggers IbeA-dependent activation of the vimentin signaling pathway at the host cell membrane. IbeA binds to its receptor Vim and co-receptor PSF that interact with α7n nAChR through lipid rafts. These communications trigger phosphorylation of signaling proteins (e.g., Vim, TAK1), which in turn activates the nuclear factor-kappaB (NF-κB) pathways via activation of the IκB kinase (IKK) complex. NF-κB activation resulted to the nuclear translocation of NF-κB, which induces the production of cytokines, chemokines, and others proinflammatory molecules in response to bacterial stimuli.

Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a RPAb against α7 nAChR from Genescript (Piscataway, NJ) and a rat anti-mouse Ly-6G (Gr-1) antibody from eBiosciences (San Diego, CA).

Techniques: Infection, Activation Assay, Membrane, Phospho-proteomics, Translocation Assay

Expression levels of α7 nAChR and Aβ in the brains of patients with AD and normal brains. (A) Images of the immunofluorescence double staining in the control and AD groups. (B) Aβ is expressed in the cytoplasm and extracellular matrix of cells. It was also found highly expressed in the brain slices of patients with AD, whereas the expression levels were minimal in healthy control brain sections following immunofluorescence double staining. (C) α7 nAChR was found expressed in the cytoplasm and reduced expression levels were observed in brain sections of patients with AD compared with healthy human brain sections, following immunofluorescence double staining. The cell nuclei are stained in blue using DAPI. Aβ-positive neurons are indicated in red and α3 nAChR-positive neurons are green. Scale bar, 20 µm. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control group. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease; IOD, integrated optical density.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Expression levels of α7 nAChR and Aβ in the brains of patients with AD and normal brains. (A) Images of the immunofluorescence double staining in the control and AD groups. (B) Aβ is expressed in the cytoplasm and extracellular matrix of cells. It was also found highly expressed in the brain slices of patients with AD, whereas the expression levels were minimal in healthy control brain sections following immunofluorescence double staining. (C) α7 nAChR was found expressed in the cytoplasm and reduced expression levels were observed in brain sections of patients with AD compared with healthy human brain sections, following immunofluorescence double staining. The cell nuclei are stained in blue using DAPI. Aβ-positive neurons are indicated in red and α3 nAChR-positive neurons are green. Scale bar, 20 µm. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control group. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease; IOD, integrated optical density.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Expressing, Immunofluorescence, Double Staining, Control, Staining, Standard Deviation

Mean IOD of α7 nAChR is negatively correlated with the mean IOD of Aβ in the brain of patients with AD. Mean IOD of α7 nAChR and Aβ were found to be negatively correlated with each other in the (A) temporal cortex, (B) frontal cortex and (C) hippocampus following immunofluorescence double staining of brain slices of patients with AD. Data was obtained using correlation analysis (n=9). P<0.05 α7 nAChR vs. Aβ. IOD, integrated optical density; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Mean IOD of α7 nAChR is negatively correlated with the mean IOD of Aβ in the brain of patients with AD. Mean IOD of α7 nAChR and Aβ were found to be negatively correlated with each other in the (A) temporal cortex, (B) frontal cortex and (C) hippocampus following immunofluorescence double staining of brain slices of patients with AD. Data was obtained using correlation analysis (n=9). P<0.05 α7 nAChR vs. Aβ. IOD, integrated optical density; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Immunofluorescence, Double Staining

Expression levels of α7 nAChR mRNA and protein in SH-SY5Y cells in which α7 nAChR is overexpressed or silenced. (A) mRNA and (B) protein expression levels of α7 nAChR in SH-SY5Y cells overexpressing α7 nAChR. (C) mRNA and (D) protein expression levels of α7 nAChR in SH-SY5Y cells with silenced α7 nAChR expression. β-actin was used as an internal standard. Expression levels were determined using reverse transcription-quantitative PCR and western blotting. Data are presented as the mean ± standard deviation (n=9).**P<0.01 vs. control. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Expression levels of α7 nAChR mRNA and protein in SH-SY5Y cells in which α7 nAChR is overexpressed or silenced. (A) mRNA and (B) protein expression levels of α7 nAChR in SH-SY5Y cells overexpressing α7 nAChR. (C) mRNA and (D) protein expression levels of α7 nAChR in SH-SY5Y cells with silenced α7 nAChR expression. β-actin was used as an internal standard. Expression levels were determined using reverse transcription-quantitative PCR and western blotting. Data are presented as the mean ± standard deviation (n=9).**P<0.01 vs. control. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, Control, shRNA

Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells overexpressing α7 nAChR or with silenced α7 nAChR expression. Expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells overexpressing α7 nAChR or with silenced α7 nAChR expression. Expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, Standard Deviation, Control, shRNA

Concentration of ACh and the activity of AChE in SH-SY5Y cells in which expression of  α7   nAChR  was overexpressed or silenced.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Concentration of ACh and the activity of AChE in SH-SY5Y cells in which expression of α7 nAChR was overexpressed or silenced.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Concentration Assay, Activity Assay, Expressing, Control, shRNA, Plasmid Preparation

Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells following the overexpression of α7 nAChR or silencing of α7 nAChR, and exposure to AβO. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. The expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control; ## P<0.01, # P<0.05 vs. empty plasmid. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells following the overexpression of α7 nAChR or silencing of α7 nAChR, and exposure to AβO. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. The expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control; ## P<0.01, # P<0.05 vs. empty plasmid. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Expressing, Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, Control, Plasmid Preparation, shRNA

Apoptotic rate of SH-SY5Y cells, which are simultaneously exposed to α7 nAChR overexpression or gene silencing and AβO. (A) Apoptotic rate was determined using flow cytometry and (B) data are presented as the mean ± standard deviation (n=9). **P<0.01 vs. control; # P<0.05 vs. control + AβO. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.

Journal: Molecular Medicine Reports

Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells

doi: 10.3892/mmr.2020.11253

Figure Lengend Snippet: Apoptotic rate of SH-SY5Y cells, which are simultaneously exposed to α7 nAChR overexpression or gene silencing and AβO. (A) Apoptotic rate was determined using flow cytometry and (B) data are presented as the mean ± standard deviation (n=9). **P<0.01 vs. control; # P<0.05 vs. control + AβO. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.

Article Snippet: The anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX10096), anti-α7 nAChR rabbit polyclonal antibody (cat. no. GTX64511), fluorescent FITC-conjugated anti-rabbit IgG antibody (cat. no. BA1105), fluorescence Cy3-conjugated anti-mouse IgG antibody (cat. no. BA1031), anti-SNAP-25 rabbit monoclonal antibody (cat. no. GTX62566) and the anti-SD-95 rabbit monoclonal antibody (cat. no. GTX61948) were all purchased from GeneTex, Inc.

Techniques: Over Expression, Flow Cytometry, Standard Deviation, Control, shRNA

Nicotine activation of ERK2 in hippocampal slices is mediated by α7 nAChRs. a, Quantitative immunoblot demonstrates that 500 μm nicotine stimulated ERK2 MAPK activity, which is antagonized by 1 μm MLA in hippocampal slices from mice heterozygous for the L250T α7 nAChR transgene. Basal, 1.00 ± 0.22; nicotine (nic), 2.33 ± 0.13; MLA + nicotine, 1.34 ± 0.14. *Significant difference from basal level; p < 0.01, post hocTukey multiple comparison test. Representative immunoblot results are depicted below the response histogram. ERK1 (topband) activation paralleled that of ERK2; however, absolute levels of phospho-ERK1 were far below ERK2 and were not quantified. Slices from wild-type animals did not exhibit significant ERK2 MAPK activation with nicotine treatment, likely because of the rapid desensitization kinetics of wild-type α7 nAChRs precluding biochemical detection of ERK2 MAPK activation (Seguela et al., 1995). b, Quantitative immunoblot demonstrates that ERK2 MAPK activation by nicotine in cultured rat hippocampal slices is blocked by 1 μm MLA. Basal, 1.01 ± 0.08; nicotine, 1.66 ± 0.13; MLA + nicotine, 1.22 ± 0.09. *Denotes nicotine stimulation is significantly different from basal level;p < 0.001, post hoc Tukey multiple comparison test. Representative immunoblot results are depictedbelow the response histogram.

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: Nicotine activation of ERK2 in hippocampal slices is mediated by α7 nAChRs. a, Quantitative immunoblot demonstrates that 500 μm nicotine stimulated ERK2 MAPK activity, which is antagonized by 1 μm MLA in hippocampal slices from mice heterozygous for the L250T α7 nAChR transgene. Basal, 1.00 ± 0.22; nicotine (nic), 2.33 ± 0.13; MLA + nicotine, 1.34 ± 0.14. *Significant difference from basal level; p < 0.01, post hocTukey multiple comparison test. Representative immunoblot results are depicted below the response histogram. ERK1 (topband) activation paralleled that of ERK2; however, absolute levels of phospho-ERK1 were far below ERK2 and were not quantified. Slices from wild-type animals did not exhibit significant ERK2 MAPK activation with nicotine treatment, likely because of the rapid desensitization kinetics of wild-type α7 nAChRs precluding biochemical detection of ERK2 MAPK activation (Seguela et al., 1995). b, Quantitative immunoblot demonstrates that ERK2 MAPK activation by nicotine in cultured rat hippocampal slices is blocked by 1 μm MLA. Basal, 1.01 ± 0.08; nicotine, 1.66 ± 0.13; MLA + nicotine, 1.22 ± 0.09. *Denotes nicotine stimulation is significantly different from basal level;p < 0.001, post hoc Tukey multiple comparison test. Representative immunoblot results are depictedbelow the response histogram.

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Activation Assay, Western Blot, Activity Assay, Comparison, Cell Culture

α7 nAChR is upregulated in hippocampus and DG of Tg2576 mice. a, Quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus reveals upregulation of α7 nAChR protein as early as 4 months. *Significantly higher α7 nAChR level than age-matched control animals (p < 0.03) by Student's ttest. Dashed line represents normalized control animal level; note the change in scale for ∼20 month animals. Filled bar, CA1; shaded bar, DG. b, Representative immunoblot for α7 nAChR level in Tg2576 and age-matched control animals.

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: α7 nAChR is upregulated in hippocampus and DG of Tg2576 mice. a, Quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus reveals upregulation of α7 nAChR protein as early as 4 months. *Significantly higher α7 nAChR level than age-matched control animals (p < 0.03) by Student's ttest. Dashed line represents normalized control animal level; note the change in scale for ∼20 month animals. Filled bar, CA1; shaded bar, DG. b, Representative immunoblot for α7 nAChR level in Tg2576 and age-matched control animals.

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Western Blot, Control

Downstream targets of α7 nAChR activation in Tg2576 hippocampus exhibit dysregulation. ERK2 and CREB proteins undergo hyperactivation, followed by downregulation, as compared with age-matched control animals. Differences between Tg2576 and age-matched control animals were detected by quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus. Samples were evaluated for total and phospho-ERK2 MAPK (a, c) and total and phospho-CREB (b, d) levels in CA1 and DG, respectively. *Significant difference from age-matched control animal level (p ≤ 0.05) by Student'st test. Dashed line represents normalized control animal level. Filled bar, Total; shaded bar, phospho.

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: Downstream targets of α7 nAChR activation in Tg2576 hippocampus exhibit dysregulation. ERK2 and CREB proteins undergo hyperactivation, followed by downregulation, as compared with age-matched control animals. Differences between Tg2576 and age-matched control animals were detected by quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus. Samples were evaluated for total and phospho-ERK2 MAPK (a, c) and total and phospho-CREB (b, d) levels in CA1 and DG, respectively. *Significant difference from age-matched control animal level (p ≤ 0.05) by Student'st test. Dashed line represents normalized control animal level. Filled bar, Total; shaded bar, phospho.

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Activation Assay, Control, Western Blot

Data summary for the parameters measured in hippocampi of Tg2576 mice at different ages as compared with age-matched control animals

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: Data summary for the parameters measured in hippocampi of Tg2576 mice at different ages as compared with age-matched control animals

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Control

Animals with elevated α7 nAChR level fail to perform to criteria in the Morris water maze. Scatter plot of the third probe trial performance of individual ∼20-month-old Tg2576 and control animals versus α7 nAChR protein levels in CA1 and DG.Dashed line indicates performance criterion.Filled squares, Control; filled diamonds, Tg.

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: Animals with elevated α7 nAChR level fail to perform to criteria in the Morris water maze. Scatter plot of the third probe trial performance of individual ∼20-month-old Tg2576 and control animals versus α7 nAChR protein levels in CA1 and DG.Dashed line indicates performance criterion.Filled squares, Control; filled diamonds, Tg.

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Control

Chronic exposure to Aβ42 leads to increased α7 nAChR protein in hippocampal slice cultures. Cultured rat hippocampal slices were exposed to 100 pm Aβ42 for 144 hr, and α7 nAChR protein was quantified by immunoblot. The data that are expressed are normalized to the α7 nAChR protein level in cultures that were left untreated. Representative immunoblot results are shownbelow the histogram. *Significant difference from control level (p < 0.0001) by Student'st test. Basal, 1.00 ± 0.11; Aβ42-treated, 2.35 ± 0.13.

Journal: The Journal of Neuroscience

Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

doi: 10.1523/JNEUROSCI.21-12-04125.2001

Figure Lengend Snippet: Chronic exposure to Aβ42 leads to increased α7 nAChR protein in hippocampal slice cultures. Cultured rat hippocampal slices were exposed to 100 pm Aβ42 for 144 hr, and α7 nAChR protein was quantified by immunoblot. The data that are expressed are normalized to the α7 nAChR protein level in cultures that were left untreated. Representative immunoblot results are shownbelow the histogram. *Significant difference from control level (p < 0.0001) by Student'st test. Basal, 1.00 ± 0.11; Aβ42-treated, 2.35 ± 0.13.

Article Snippet: Anti-α7 nAChR antibody was purchased from Babco (Richmond, CA).

Techniques: Cell Culture, Western Blot, Control