il 24 antibody Search Results


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Ang-1 activates the Akt pathway in neurons through both Tie-2 and <t>β1-integrin</t> signaling. (A) RCNs were treated with Ang-1 for the indicated time. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against Tie-2, phosphor-Tie2 (Y992), β1-integrin, FAK, phosphor-FAK (Tyr397), phospho-Akt (Ser473), phosphor-GSK3α/β, and β-actin. (B) Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared to control untreated levels. Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^^p < 0.001 versus etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; GSK3α/β, glycogen synthase kinase 3α/β; RCNs, rat cortical neurons; SDS, sodium dodecyl sulfate; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.
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Ang-1 activates the Akt pathway in neurons through both Tie-2 and <t>β1-integrin</t> signaling. (A) RCNs were treated with Ang-1 for the indicated time. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against Tie-2, phosphor-Tie2 (Y992), β1-integrin, FAK, phosphor-FAK (Tyr397), phospho-Akt (Ser473), phosphor-GSK3α/β, and β-actin. (B) Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared to control untreated levels. Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^^p < 0.001 versus etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; GSK3α/β, glycogen synthase kinase 3α/β; RCNs, rat cortical neurons; SDS, sodium dodecyl sulfate; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.
Antibody Against Il 24, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems il24 r d systems 283123 igg2b
Ang-1 activates the Akt pathway in neurons through both Tie-2 and <t>β1-integrin</t> signaling. (A) RCNs were treated with Ang-1 for the indicated time. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against Tie-2, phosphor-Tie2 (Y992), β1-integrin, FAK, phosphor-FAK (Tyr397), phospho-Akt (Ser473), phosphor-GSK3α/β, and β-actin. (B) Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared to control untreated levels. Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^^p < 0.001 versus etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; GSK3α/β, glycogen synthase kinase 3α/β; RCNs, rat cortical neurons; SDS, sodium dodecyl sulfate; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.
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Image Search Results


Ang-1 activates the Akt pathway in neurons through both Tie-2 and β1-integrin signaling. (A) RCNs were treated with Ang-1 for the indicated time. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against Tie-2, phosphor-Tie2 (Y992), β1-integrin, FAK, phosphor-FAK (Tyr397), phospho-Akt (Ser473), phosphor-GSK3α/β, and β-actin. (B) Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared to control untreated levels. Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^^p < 0.001 versus etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; GSK3α/β, glycogen synthase kinase 3α/β; RCNs, rat cortical neurons; SDS, sodium dodecyl sulfate; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.

Journal: Journal of Neurotrauma

Article Title: MicroRNA-711–Induced Downregulation of Angiopoietin-1 Mediates Neuronal Cell Death

doi: 10.1089/neu.2017.5572

Figure Lengend Snippet: Ang-1 activates the Akt pathway in neurons through both Tie-2 and β1-integrin signaling. (A) RCNs were treated with Ang-1 for the indicated time. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against Tie-2, phosphor-Tie2 (Y992), β1-integrin, FAK, phosphor-FAK (Tyr397), phospho-Akt (Ser473), phosphor-GSK3α/β, and β-actin. (B) Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared to control untreated levels. Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^^p < 0.001 versus etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; GSK3α/β, glycogen synthase kinase 3α/β; RCNs, rat cortical neurons; SDS, sodium dodecyl sulfate; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.

Article Snippet: The following antibodies were used in this study: Histone H2A.X (ab11175; Abcam); apoptosis-inducing factor (AIF; sc-13116); cytochrome c (sc-13560) and Bim (sc-11425; Santa Cruz Biotechnology, Santa Cruz, CA); cleaved caspase-3 (#9661), cleaved PARP (poly (ADP-ribose) polymerase-1; #9545); phospho-GSK3α/β (glycogen synthase kinase 3α/β; Ser21/9; #9331); forkhead box O3a (FoxO3a; 75D8; #2497); Akt (pan; 11E7; #4685); FAK (#3285); phospho-FAK (Tyr397; #3283); phospho-p53 (Ser15; #9284); p53 (#2524); mitogen-activated protein kinase kinase 1 and 2 (MEK1/2; #8727); Lamin A/C (#4777); cyclooxegenase IV (COX-IV; #4844); phospho-Akt (Ser473; #4060; Cell Signaling Technology; GAPDH (ADI-CSA-335) and α-fodrin (BML-FG6090); active Bax (ALX-804-224-C100; Enzo Life Sciences, Inc., Farmingdale, NY); PUMA (#3041), Noxa (#2437; ProSci Incorporated, Poway, CA); β-actin (A1978); MAP2 (M3696; Sigma-Aldrich); integrin β1 (MAB1965); GFAP (MAB360; Millipore, Billerica, MA); Ang-1 (GTX28451; GeneTex Inc., Irvine, CA); Tie-2 (#AF762); phospho-Tie-2 (#AF2720; R&D Systems); and ionized calcium-binding adaptor molecule 1 (019-19741; Wako Pure Chemical Industries, Osaka, Japan).

Techniques: Control

Blocking of Tie-2 and β1-integrin signaling inhibits the neuroprotective effect of Ang-1. RCNs were treated for 30 min with antibodies against Tie2 (50 μg/mL; A); antibodies against β1-integrin (5 μg/mL; B); combination of Tie2 (50 μg/mL) and β1-integrin (5 μg/mL; C) and FAK inhibitor PF573228 (100 nM; D). Next RCNs were treated with Ang-1 and etoposide (Etop) or etoposide alone. Twenty-four hours later, LDH release was measured. Data are expressed as percentage of control untreated neurons. (E) RCNs were treated with etoposide alone; Ang-1 and etoposide and etoposide; and Ang-1 etoposide and Akt inhibitor (2.875 μM). Cell death and cell viability were measured using the LDH and Calcein AM (calcein-acetoxymethyl ester). Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^p < 0.01; ^^^p < 0.001 versus etoposide treated; #p < 0.05; ##p < 0.01; ###p < 0.001 versus Ang-1 + etoposide treated; ∼∼p < 0.01; ∼∼∼p < 0.001 versus Tie-2 blocking/Ang-1/etoposide treated; &&p < 0.01 versus β1-integrin blocking/Ang-1/etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; LDH, lactate dehydrogenase; RCNs, rat cortical neurons; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.

Journal: Journal of Neurotrauma

Article Title: MicroRNA-711–Induced Downregulation of Angiopoietin-1 Mediates Neuronal Cell Death

doi: 10.1089/neu.2017.5572

Figure Lengend Snippet: Blocking of Tie-2 and β1-integrin signaling inhibits the neuroprotective effect of Ang-1. RCNs were treated for 30 min with antibodies against Tie2 (50 μg/mL; A); antibodies against β1-integrin (5 μg/mL; B); combination of Tie2 (50 μg/mL) and β1-integrin (5 μg/mL; C) and FAK inhibitor PF573228 (100 nM; D). Next RCNs were treated with Ang-1 and etoposide (Etop) or etoposide alone. Twenty-four hours later, LDH release was measured. Data are expressed as percentage of control untreated neurons. (E) RCNs were treated with etoposide alone; Ang-1 and etoposide and etoposide; and Ang-1 etoposide and Akt inhibitor (2.875 μM). Cell death and cell viability were measured using the LDH and Calcein AM (calcein-acetoxymethyl ester). Data represent the mean ± SEM. One-way ANOVA, SNK post-hoc analysis; *p < 0.05; **p < 0.01; ***p < 0.001 versus cnt; ^^p < 0.01; ^^^p < 0.001 versus etoposide treated; #p < 0.05; ##p < 0.01; ###p < 0.001 versus Ang-1 + etoposide treated; ∼∼p < 0.01; ∼∼∼p < 0.001 versus Tie-2 blocking/Ang-1/etoposide treated; &&p < 0.01 versus β1-integrin blocking/Ang-1/etoposide treated (N = 3). Akt, protein kinase B; Ang-1, angiopoietin-1; ANOVA, analysis of variance; FAK, focal adhesion kinase; LDH, lactate dehydrogenase; RCNs, rat cortical neurons; SEM, standard error of the mean; SNK, Student–Newman–Keuls; Tie-2, Tunica interna endothelial cell kinase 2.

Article Snippet: The following antibodies were used in this study: Histone H2A.X (ab11175; Abcam); apoptosis-inducing factor (AIF; sc-13116); cytochrome c (sc-13560) and Bim (sc-11425; Santa Cruz Biotechnology, Santa Cruz, CA); cleaved caspase-3 (#9661), cleaved PARP (poly (ADP-ribose) polymerase-1; #9545); phospho-GSK3α/β (glycogen synthase kinase 3α/β; Ser21/9; #9331); forkhead box O3a (FoxO3a; 75D8; #2497); Akt (pan; 11E7; #4685); FAK (#3285); phospho-FAK (Tyr397; #3283); phospho-p53 (Ser15; #9284); p53 (#2524); mitogen-activated protein kinase kinase 1 and 2 (MEK1/2; #8727); Lamin A/C (#4777); cyclooxegenase IV (COX-IV; #4844); phospho-Akt (Ser473; #4060; Cell Signaling Technology; GAPDH (ADI-CSA-335) and α-fodrin (BML-FG6090); active Bax (ALX-804-224-C100; Enzo Life Sciences, Inc., Farmingdale, NY); PUMA (#3041), Noxa (#2437; ProSci Incorporated, Poway, CA); β-actin (A1978); MAP2 (M3696; Sigma-Aldrich); integrin β1 (MAB1965); GFAP (MAB360; Millipore, Billerica, MA); Ang-1 (GTX28451; GeneTex Inc., Irvine, CA); Tie-2 (#AF762); phospho-Tie-2 (#AF2720; R&D Systems); and ionized calcium-binding adaptor molecule 1 (019-19741; Wako Pure Chemical Industries, Osaka, Japan).

Techniques: Blocking Assay, Control