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antibodies against p tak1 thr 184 187 (Cell Signaling Technology Inc)

Name: antibodies against p tak1 thr 184 187
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Cell Signaling Technology Inc antibodies against p tak1 thr 184 187
<t>TAK1</t> regulates IL-1β-induced IL-6 and IL-8 production in RASF. (A, B) RASFs were pretreated with PGG (5 µM) for 2 hr, followed by IL-1β (10 ng/ml) stimulation for 24 hours. Cytokines array was done as per instruction and developed on X-ray and analyzed with ChemiDoc™ scanning for intensity (A, B, <xref ref-type=

<t>TAK1</t> regulates IL-1β-induced IL-6 and IL-8 production in RASF. (A, B) RASFs were pretreated with PGG (5 µM) for 2 hr, followed by IL-1β (10 ng/ml) stimulation for 24 hours. Cytokines array was done as per instruction and developed on X-ray and analyzed with ChemiDoc™ scanning for intensity (A, B, <xref ref-type=

antibodies against p tak1 thr 184 187 - by Bioz Stars, 2026-02

93/100 stars

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1) Product Images from "Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model"

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2022.928436

TAK1 regulates IL-1β-induced IL-6 and IL-8 production in RASF. (A, B) RASFs were pretreated with PGG (5 µM) for 2 hr, followed by IL-1β (10 ng/ml) stimulation for 24 hours. Cytokines array was done as per instruction and developed on X-ray and analyzed with ChemiDoc™ scanning for intensity (A, B, <xref ref-type=

S1 ) IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. (C, D) RANTES and MMP-1 (E, F) . The values are represented as mean ± SEM of n=4 experiments using different donors. **p<0.01 for IL-1β vs IL-1β+PGG. " title="TAK1 regulates IL-1β-induced IL-6 and IL-8 production in RASF. ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: TAK1 regulates IL-1β-induced IL-6 and IL-8 production in RASF. (A, B) RASFs were pretreated with PGG (5 µM) for 2 hr, followed by IL-1β (10 ng/ml) stimulation for 24 hours. Cytokines array was done as per instruction and developed on X-ray and analyzed with ChemiDoc™ scanning for intensity (A, B, S1 ) IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. (C, D) RANTES and MMP-1 (E, F) . The values are represented as mean ± SEM of n=4 experiments using different donors. **p<0.01 for IL-1β vs IL-1β+PGG.

Techniques Used: Enzyme-linked Immunosorbent Assay

PGG selectively inhibits phosphorylation of TAK1 at the Thr184/187 site to inhibit its kinase activity. (A) RASF was pretreated with PGG (1-5 µM) for 2 hr, followed by IL-1β stimulation for 30 minutes. Cell lysates were analyzed for MYD88, IRAK-1, IRAK-M, CYLD, A20, TAB1, pTAK1 (Thr 184/187 ), TAK1, TRAF6, I-kBα, p38, pJNK, p-c-Jun, and β-actin. (B) PBMC were pretreated with PGG (5 µM), followed by stimulation with a TLR2 agonist (PamCys3, 1 µg/ml), or TLR4 agonist (lipopolysaccharide, LPS; 1 µg/ml), IL-6 and IL-8 IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. The results in each figure represent the experiments repeated on four RASF from different donors. (C) RASFs pretreated with PGG (10 μM) and stimulated with IL-1β, immunoprecipitated (IP) with O-GlcNAc or TAB1, and probe for TAK1, TAB1, and p65, also included input for O-GlcNAc to show equal loading. #p<0.05 IL-1b vs. IL-1b+PGG; **p<0.01 for IL-1β vs IL-1β+ PGG.

Figure Legend Snippet: PGG selectively inhibits phosphorylation of TAK1 at the Thr184/187 site to inhibit its kinase activity. (A) RASF was pretreated with PGG (1-5 µM) for 2 hr, followed by IL-1β stimulation for 30 minutes. Cell lysates were analyzed for MYD88, IRAK-1, IRAK-M, CYLD, A20, TAB1, pTAK1 (Thr 184/187 ), TAK1, TRAF6, I-kBα, p38, pJNK, p-c-Jun, and β-actin. (B) PBMC were pretreated with PGG (5 µM), followed by stimulation with a TLR2 agonist (PamCys3, 1 µg/ml), or TLR4 agonist (lipopolysaccharide, LPS; 1 µg/ml), IL-6 and IL-8 IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. The results in each figure represent the experiments repeated on four RASF from different donors. (C) RASFs pretreated with PGG (10 μM) and stimulated with IL-1β, immunoprecipitated (IP) with O-GlcNAc or TAB1, and probe for TAK1, TAB1, and p65, also included input for O-GlcNAc to show equal loading. #p<0.05 IL-1b vs. IL-1b+PGG; **p<0.01 for IL-1β vs IL-1β+ PGG.

Techniques Used: Phospho-proteomics, Activity Assay, Enzyme-linked Immunosorbent Assay, Immunoprecipitation

Unique insights from the in silico molecular docking studies of PGG binding in the TAK1-TAB1 complex. (A) Molecular dynamics conformation at 50 ns of PGG in the binding site of TAK1-TAB1 complex. Residue properties surface shown in the Red, Blue and Green represent electronegative, electropositive, and hydrophobic surface area of the binding site. The H-bonds are shown as a dotted line. (B) Inhibition of the TAK-1 in vitro kinase activity by PGG was tested using a kinase assay as per the manufacturer’s instructions. **p<0.01 for No ATP vs ATP. #p<0.05 and ##p<0.01 for ATP vs. PGG.

Figure Legend Snippet: Unique insights from the in silico molecular docking studies of PGG binding in the TAK1-TAB1 complex. (A) Molecular dynamics conformation at 50 ns of PGG in the binding site of TAK1-TAB1 complex. Residue properties surface shown in the Red, Blue and Green represent electronegative, electropositive, and hydrophobic surface area of the binding site. The H-bonds are shown as a dotted line. (B) Inhibition of the TAK-1 in vitro kinase activity by PGG was tested using a kinase assay as per the manufacturer’s instructions. **p<0.01 for No ATP vs ATP. #p<0.05 and ##p<0.01 for ATP vs. PGG.

Techniques Used: In Silico, Binding Assay, Residue, Inhibition, In Vitro, Activity Assay, Kinase Assay

PGG modulates phosphorylation of TAK-1 activity in vivo . (A) H&E staining of rat ankles obtained from normal rats, rats given AIA, and rats were given AIA and Penta-O-galloyl-β-D-glucose (PGG) shows inflammation. In addition, pTAK1 and TAK1 were immunolocalized via IHC staining. (A) Naïve rat ankle stained via H&E shows no inflammation and synoviocytes (SNC), lymphocytes (L), bone (B), and macrophages (M) are present. (B) AIA rat ankle stained by H&E shows high amounts of inflammation including the presence of endothelial cells (EC) which comprise blood vessels (BV) and many synoviocytes (SNC), lymphocytes (L), and macrophages (M). (C) AIA+ PGG rat ankles stained by H&E shows low levels of inflammation and that endothelial cells (EC), blood vessels (BV), synoviocytes (SNC), lymphocytes (L), and macrophages (M) are present. (D) There is no staining for TAK1 in naïve rat ankles. (E) There is minimal staining in synoviocytes (SNC) in AIA rat ankles. (F) There is minimal staining in synoviocytes (SNC) in AIA+PGG rat ankles. (G) There is no staining for p-TAK-1 in naïve rat ankles. (H) There is intense staining for p-TAK-1 in macrophages (M), synoviocytes (SNC), and lymphocytes (L). (I) There is a minimal staining in macrophages (M), synoviocytes (SNC), and lymphocytes (L). NOTE: the same tissue of each treatment was incubated with nonspecific IgG, which showed no expression. (Original magnification × 40). (B) Joint homogenates (30 µg per sample) from naïve, AIA, and PGG treated rats were analyzed for the expression of IRAK-1 (Thr 209 ), pTAK1 (Thr 184/187 ), TAK1, TRAF6, and β-actin.

Figure Legend Snippet: PGG modulates phosphorylation of TAK-1 activity in vivo . (A) H&E staining of rat ankles obtained from normal rats, rats given AIA, and rats were given AIA and Penta-O-galloyl-β-D-glucose (PGG) shows inflammation. In addition, pTAK1 and TAK1 were immunolocalized via IHC staining. (A) Naïve rat ankle stained via H&E shows no inflammation and synoviocytes (SNC), lymphocytes (L), bone (B), and macrophages (M) are present. (B) AIA rat ankle stained by H&E shows high amounts of inflammation including the presence of endothelial cells (EC) which comprise blood vessels (BV) and many synoviocytes (SNC), lymphocytes (L), and macrophages (M). (C) AIA+ PGG rat ankles stained by H&E shows low levels of inflammation and that endothelial cells (EC), blood vessels (BV), synoviocytes (SNC), lymphocytes (L), and macrophages (M) are present. (D) There is no staining for TAK1 in naïve rat ankles. (E) There is minimal staining in synoviocytes (SNC) in AIA rat ankles. (F) There is minimal staining in synoviocytes (SNC) in AIA+PGG rat ankles. (G) There is no staining for p-TAK-1 in naïve rat ankles. (H) There is intense staining for p-TAK-1 in macrophages (M), synoviocytes (SNC), and lymphocytes (L). (I) There is a minimal staining in macrophages (M), synoviocytes (SNC), and lymphocytes (L). NOTE: the same tissue of each treatment was incubated with nonspecific IgG, which showed no expression. (Original magnification × 40). (B) Joint homogenates (30 µg per sample) from naïve, AIA, and PGG treated rats were analyzed for the expression of IRAK-1 (Thr 209 ), pTAK1 (Thr 184/187 ), TAK1, TRAF6, and β-actin.

Techniques Used: Phospho-proteomics, Activity Assay, In Vivo, Staining, Immunohistochemistry, Incubation, Expressing

Schematic figure showing the mechanism of PGG in IL1β signaling. In IL1β signaling, IL-1β activates the signal through its receptor to MyD88, an adaptor protein which further recruits IRAK1-4 and activates TAK1 dependent inflammation. We showed that PGG suppresses IL-1β-induced post translation modification (O-GlcNAC) and downstream inflammatory responses by inhibiting multiple cytokines.

Figure Legend Snippet: Schematic figure showing the mechanism of PGG in IL1β signaling. In IL1β signaling, IL-1β activates the signal through its receptor to MyD88, an adaptor protein which further recruits IRAK1-4 and activates TAK1 dependent inflammation. We showed that PGG suppresses IL-1β-induced post translation modification (O-GlcNAC) and downstream inflammatory responses by inhibiting multiple cytokines.

Techniques Used: Post Translation Modification

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Image Search Results

Journal: Frontiers in Immunology

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

doi: 10.3389/fimmu.2022.928436

Figure Lengend Snippet: TAK1 regulates IL-1β-induced IL-6 and IL-8 production in RASF. (A, B) RASFs were pretreated with PGG (5 µM) for 2 hr, followed by IL-1β (10 ng/ml) stimulation for 24 hours. Cytokines array was done as per instruction and developed on X-ray and analyzed with ChemiDoc™ scanning for intensity (A, B, S1 ) IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. (C, D) RANTES and MMP-1 (E, F) . The values are represented as mean ± SEM of n=4 experiments using different donors. **p<0.01 for IL-1β vs IL-1β+PGG.

Article Snippet: Antibodies against p-TAK1 Thr 184/187 (#4531), p-JNK (#9251) p-JNK (#4511), p-c-Jun (Ser 73 ) (#9164), MyD88 (D80F5) (#4283), CYLD (D6O5O) (#12797) were purchased from Cell Signaling Technology (Beverly, MA).

Techniques: Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

doi: 10.3389/fimmu.2022.928436

Figure Lengend Snippet: PGG selectively inhibits phosphorylation of TAK1 at the Thr184/187 site to inhibit its kinase activity. (A) RASF was pretreated with PGG (1-5 µM) for 2 hr, followed by IL-1β stimulation for 30 minutes. Cell lysates were analyzed for MYD88, IRAK-1, IRAK-M, CYLD, A20, TAB1, pTAK1 (Thr 184/187 ), TAK1, TRAF6, I-kBα, p38, pJNK, p-c-Jun, and β-actin. (B) PBMC were pretreated with PGG (5 µM), followed by stimulation with a TLR2 agonist (PamCys3, 1 µg/ml), or TLR4 agonist (lipopolysaccharide, LPS; 1 µg/ml), IL-6 and IL-8 IL-6 and IL-8 production was determined in the conditioned media using commercially available ELISA kits. The results in each figure represent the experiments repeated on four RASF from different donors. (C) RASFs pretreated with PGG (10 μM) and stimulated with IL-1β, immunoprecipitated (IP) with O-GlcNAc or TAB1, and probe for TAK1, TAB1, and p65, also included input for O-GlcNAc to show equal loading. #p<0.05 IL-1b vs. IL-1b+PGG; **p<0.01 for IL-1β vs IL-1β+ PGG.

Techniques: Phospho-proteomics, Activity Assay, Enzyme-linked Immunosorbent Assay, Immunoprecipitation

Journal: Frontiers in Immunology

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

doi: 10.3389/fimmu.2022.928436

Figure Lengend Snippet: Unique insights from the in silico molecular docking studies of PGG binding in the TAK1-TAB1 complex. (A) Molecular dynamics conformation at 50 ns of PGG in the binding site of TAK1-TAB1 complex. Residue properties surface shown in the Red, Blue and Green represent electronegative, electropositive, and hydrophobic surface area of the binding site. The H-bonds are shown as a dotted line. (B) Inhibition of the TAK-1 in vitro kinase activity by PGG was tested using a kinase assay as per the manufacturer’s instructions. **p<0.01 for No ATP vs ATP. #p<0.05 and ##p<0.01 for ATP vs. PGG.

Techniques: In Silico, Binding Assay, Residue, Inhibition, In Vitro, Activity Assay, Kinase Assay

Journal: Frontiers in Immunology

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

doi: 10.3389/fimmu.2022.928436

Figure Lengend Snippet: PGG modulates phosphorylation of TAK-1 activity in vivo . (A) H&E staining of rat ankles obtained from normal rats, rats given AIA, and rats were given AIA and Penta-O-galloyl-β-D-glucose (PGG) shows inflammation. In addition, pTAK1 and TAK1 were immunolocalized via IHC staining. (A) Naïve rat ankle stained via H&E shows no inflammation and synoviocytes (SNC), lymphocytes (L), bone (B), and macrophages (M) are present. (B) AIA rat ankle stained by H&E shows high amounts of inflammation including the presence of endothelial cells (EC) which comprise blood vessels (BV) and many synoviocytes (SNC), lymphocytes (L), and macrophages (M). (C) AIA+ PGG rat ankles stained by H&E shows low levels of inflammation and that endothelial cells (EC), blood vessels (BV), synoviocytes (SNC), lymphocytes (L), and macrophages (M) are present. (D) There is no staining for TAK1 in naïve rat ankles. (E) There is minimal staining in synoviocytes (SNC) in AIA rat ankles. (F) There is minimal staining in synoviocytes (SNC) in AIA+PGG rat ankles. (G) There is no staining for p-TAK-1 in naïve rat ankles. (H) There is intense staining for p-TAK-1 in macrophages (M), synoviocytes (SNC), and lymphocytes (L). (I) There is a minimal staining in macrophages (M), synoviocytes (SNC), and lymphocytes (L). NOTE: the same tissue of each treatment was incubated with nonspecific IgG, which showed no expression. (Original magnification × 40). (B) Joint homogenates (30 µg per sample) from naïve, AIA, and PGG treated rats were analyzed for the expression of IRAK-1 (Thr 209 ), pTAK1 (Thr 184/187 ), TAK1, TRAF6, and β-actin.

Techniques: Phospho-proteomics, Activity Assay, In Vivo, Staining, Immunohistochemistry, Incubation, Expressing

Journal: Frontiers in Immunology

Article Title: Penta-o-galloyl-beta-d-Glucose (PGG) inhibits inflammation in human rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis model

doi: 10.3389/fimmu.2022.928436

Figure Lengend Snippet: Schematic figure showing the mechanism of PGG in IL1β signaling. In IL1β signaling, IL-1β activates the signal through its receptor to MyD88, an adaptor protein which further recruits IRAK1-4 and activates TAK1 dependent inflammation. We showed that PGG suppresses IL-1β-induced post translation modification (O-GlcNAC) and downstream inflammatory responses by inhibiting multiple cytokines.

Techniques: Post Translation Modification