mapk9 rabbit mono cell signaling Search Results


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TIPE2 inhibited activation of NF-κB and JNK via downregulation of TAK1. A Immunofluorescence staining was performed to analyze phosphor-JNK in spinal cord and DRG after 14 days. Mean fluorescence intensity of phospho-JNK was analyzed by Image J 1.49p. The scale bar was 20 μm. B Western blot was carried out to analyze the expression of p-NF-κB p65, <t>p-JNK1,</t> and <t>p-JNK2</t> in spinal cord after 14 days. && p < 0.01 versus Sham; % p < 0.05, %% p < 0.01 versus Model; $ p < 0.05, $$ p < 0.01 versus TIPE2-1; ! p < 0.05, !! p < 0.01 versus TIPE2-5
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TIPE2 inhibited activation of NF-κB and JNK via downregulation of TAK1. A Immunofluorescence staining was performed to analyze phosphor-JNK in spinal cord and DRG after 14 days. Mean fluorescence intensity of phospho-JNK was analyzed by Image J 1.49p. The scale bar was 20 μm. B Western blot was carried out to analyze the expression of p-NF-κB p65, <t>p-JNK1,</t> and <t>p-JNK2</t> in spinal cord after 14 days. && p < 0.01 versus Sham; % p < 0.05, %% p < 0.01 versus Model; $ p < 0.05, $$ p < 0.01 versus TIPE2-1; ! p < 0.05, !! p < 0.01 versus TIPE2-5
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Fig. 5 Effects of tyrosine phosphatase inhibition on the interaction of phospho-c- Jun N-terminal kinases <t>(p-JNKs)</t> with 14-3- 3, serine phosphorylation of 14-3-3, inter- action between 14-3-3 and Bax, and mitochondrial translocation of Bax in the hippocampal CA1 region induced by cerebral ischemia–reperfusion. (a) Co- immunoprecipitation and western blotting analysis were used to explore the binding behavior of the interactions of 14-3-3 with phospho-JNK or Bax, and the alteration behavior of serine phosphorylation of 14-3- 3. Homogenates were subjected to immu- noprecipitation with anti-phospho-JNKs or anti-14-3-3 antibody and the immunocom- plexes were probed for the presence of 14- 3-3, Bax and phospho-serine. (c) Effects of pre-treatment with orthovanadate (OV) on the increased phosphorylation of 14-3-3 and the decreased interaction of 14-3-3 with Bax induced by 6 h of ischemia–reperfusion in the hippocampal CA1 region. (d) Effects of tyrosine phosphatase inhibition on the increased Bax translocation to the mito- chondria induced by 6 h of ischemia–rep- erfusion in the hippocampal CA1 region. (b, e) Bands on western blots were scanned and the data were expressed as a per- centage of the value of sham-operated rats. Values are given as the mean ± SD of four independent experiments (n ¼ 4). *p < 0.05 versus sham control. #p < 0.05, significant difference versus the vehicle- treated group. IP, immunoprecipitated; OD, optical density; WB, western blotted.
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Fig. 5 Effects of tyrosine phosphatase inhibition on the interaction of phospho-c- Jun N-terminal kinases <t>(p-JNKs)</t> with 14-3- 3, serine phosphorylation of 14-3-3, inter- action between 14-3-3 and Bax, and mitochondrial translocation of Bax in the hippocampal CA1 region induced by cerebral ischemia–reperfusion. (a) Co- immunoprecipitation and western blotting analysis were used to explore the binding behavior of the interactions of 14-3-3 with phospho-JNK or Bax, and the alteration behavior of serine phosphorylation of 14-3- 3. Homogenates were subjected to immu- noprecipitation with anti-phospho-JNKs or anti-14-3-3 antibody and the immunocom- plexes were probed for the presence of 14- 3-3, Bax and phospho-serine. (c) Effects of pre-treatment with orthovanadate (OV) on the increased phosphorylation of 14-3-3 and the decreased interaction of 14-3-3 with Bax induced by 6 h of ischemia–reperfusion in the hippocampal CA1 region. (d) Effects of tyrosine phosphatase inhibition on the increased Bax translocation to the mito- chondria induced by 6 h of ischemia–rep- erfusion in the hippocampal CA1 region. (b, e) Bands on western blots were scanned and the data were expressed as a per- centage of the value of sham-operated rats. Values are given as the mean ± SD of four independent experiments (n ¼ 4). *p < 0.05 versus sham control. #p < 0.05, significant difference versus the vehicle- treated group. IP, immunoprecipitated; OD, optical density; WB, western blotted.
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Image Search Results


Antibodies used for the detection and quantification of target proteins.

Journal: International Journal of Molecular Sciences

Article Title: Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress

doi: 10.3390/ijms24032303

Figure Lengend Snippet: Antibodies used for the detection and quantification of target proteins.

Article Snippet: JNK1/2 , Human JNK2 (GST fusion protein) , Rabbit , 9252 , 6 , Cell Signaling, USA.

Techniques:

TIPE2 inhibited activation of NF-κB and JNK via downregulation of TAK1. A Immunofluorescence staining was performed to analyze phosphor-JNK in spinal cord and DRG after 14 days. Mean fluorescence intensity of phospho-JNK was analyzed by Image J 1.49p. The scale bar was 20 μm. B Western blot was carried out to analyze the expression of p-NF-κB p65, p-JNK1, and p-JNK2 in spinal cord after 14 days. && p < 0.01 versus Sham; % p < 0.05, %% p < 0.01 versus Model; $ p < 0.05, $$ p < 0.01 versus TIPE2-1; ! p < 0.05, !! p < 0.01 versus TIPE2-5

Journal: Neurochemical Research

Article Title: Exogenous TIPE2 Inhibit TAK1 to Improve Inflammation and Neuropathic Pain Induced by Sciatic Nerve Injury Through Inactivating NF-κB and JNK

doi: 10.1007/s11064-022-03671-4

Figure Lengend Snippet: TIPE2 inhibited activation of NF-κB and JNK via downregulation of TAK1. A Immunofluorescence staining was performed to analyze phosphor-JNK in spinal cord and DRG after 14 days. Mean fluorescence intensity of phospho-JNK was analyzed by Image J 1.49p. The scale bar was 20 μm. B Western blot was carried out to analyze the expression of p-NF-κB p65, p-JNK1, and p-JNK2 in spinal cord after 14 days. && p < 0.01 versus Sham; % p < 0.05, %% p < 0.01 versus Model; $ p < 0.05, $$ p < 0.01 versus TIPE2-1; ! p < 0.05, !! p < 0.01 versus TIPE2-5

Article Snippet: The detailed information of antibodies were as followed: (1) primary antibodies: rabbit anti-rat TIPE2 polyclonal antibody (1:550, 15940-1-AP, Proteintech), rabbit anti-rat TAK1 polyclonal antibody (1:80, bs-3585R, Bioss), mouse anti-rat TAK1 antibody (1:250, 67707-1, proteintech), rabbit anti-rat p-JNK1 + JNK2 (phospho T183 + Y185) (1:150, ab131499, Abcam), mouse anti-rat GFAP monoclonal antibody (1:600, 60190-1-lg, Proteintech); (2) second antibodies: goat anti-rabbit Cy3-labeled IgG (H + L) (1:500, A0516, Beyotime), goat anti-mouse FITC-labeled IgG (H + L) (1:500, A0568, Beyotime).

Techniques: Activation Assay, Immunofluorescence, Staining, Fluorescence, Western Blot, Expressing

Fig. 5 Effects of tyrosine phosphatase inhibition on the interaction of phospho-c- Jun N-terminal kinases (p-JNKs) with 14-3- 3, serine phosphorylation of 14-3-3, inter- action between 14-3-3 and Bax, and mitochondrial translocation of Bax in the hippocampal CA1 region induced by cerebral ischemia–reperfusion. (a) Co- immunoprecipitation and western blotting analysis were used to explore the binding behavior of the interactions of 14-3-3 with phospho-JNK or Bax, and the alteration behavior of serine phosphorylation of 14-3- 3. Homogenates were subjected to immu- noprecipitation with anti-phospho-JNKs or anti-14-3-3 antibody and the immunocom- plexes were probed for the presence of 14- 3-3, Bax and phospho-serine. (c) Effects of pre-treatment with orthovanadate (OV) on the increased phosphorylation of 14-3-3 and the decreased interaction of 14-3-3 with Bax induced by 6 h of ischemia–reperfusion in the hippocampal CA1 region. (d) Effects of tyrosine phosphatase inhibition on the increased Bax translocation to the mito- chondria induced by 6 h of ischemia–rep- erfusion in the hippocampal CA1 region. (b, e) Bands on western blots were scanned and the data were expressed as a per- centage of the value of sham-operated rats. Values are given as the mean ± SD of four independent experiments (n ¼ 4). *p < 0.05 versus sham control. #p < 0.05, significant difference versus the vehicle- treated group. IP, immunoprecipitated; OD, optical density; WB, western blotted.

Journal: Journal of neurochemistry

Article Title: Akt inhibits MLK3/JNK3 signaling by inactivating Rac1: a protective mechanism against ischemic brain injury.

doi: 10.1111/j.1471-4159.2006.04020.x

Figure Lengend Snippet: Fig. 5 Effects of tyrosine phosphatase inhibition on the interaction of phospho-c- Jun N-terminal kinases (p-JNKs) with 14-3- 3, serine phosphorylation of 14-3-3, inter- action between 14-3-3 and Bax, and mitochondrial translocation of Bax in the hippocampal CA1 region induced by cerebral ischemia–reperfusion. (a) Co- immunoprecipitation and western blotting analysis were used to explore the binding behavior of the interactions of 14-3-3 with phospho-JNK or Bax, and the alteration behavior of serine phosphorylation of 14-3- 3. Homogenates were subjected to immu- noprecipitation with anti-phospho-JNKs or anti-14-3-3 antibody and the immunocom- plexes were probed for the presence of 14- 3-3, Bax and phospho-serine. (c) Effects of pre-treatment with orthovanadate (OV) on the increased phosphorylation of 14-3-3 and the decreased interaction of 14-3-3 with Bax induced by 6 h of ischemia–reperfusion in the hippocampal CA1 region. (d) Effects of tyrosine phosphatase inhibition on the increased Bax translocation to the mito- chondria induced by 6 h of ischemia–rep- erfusion in the hippocampal CA1 region. (b, e) Bands on western blots were scanned and the data were expressed as a per- centage of the value of sham-operated rats. Values are given as the mean ± SD of four independent experiments (n ¼ 4). *p < 0.05 versus sham control. #p < 0.05, significant difference versus the vehicle- treated group. IP, immunoprecipitated; OD, optical density; WB, western blotted.

Article Snippet: Antibodies to PTEN (sc-9145), Rac1 (sc-217), p-Rac1 (Ser71, sc-12924-R), MLK3 (sc-13072), active JNKs (recognizes JNK1, JNK2 and JNK3, sc-6254), Fas-L (sc-6237), Fas (sc1023), Bax (sc-493), 14-3-3 (sc-1019) and phospho-c-Jun (sc-822) were all purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

Techniques: Inhibition, Phospho-proteomics, Translocation Assay, Immunoprecipitation, Western Blot, Binding Assay, Control