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phospho p38  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc phospho p38
    Phospho P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+p38+mapk/p38gamma+MAPK+Antibody/pm42892647-235-84-85
    Average 94 stars, based on 52 article reviews
    phospho p38 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Incubation:

    Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach
    Article Snippet: Equal protein amounts were denatured, separated by 12 % SDS-PAGE, and transferred onto 0.45 μm PVDF membranes (Merck-Millipore, Burlington, MA, USA). .. Membranes were blocked with 5 % non-fat milk in TBS-T and incubated overnight at 4 °C with primary antibodies against phospho-AKT (Thr308), phospho-NFκB p65 (Ser536), phospho-p38 MAPK (Thr180/Tyr182), phospho-STAT1 (Tyr701), and phospho-STAT3 (Tyr705) (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA). .. Following washes, membranes were incubated with HRP-conjugated secondary antibodies, and signals were detected using PierceTM ECL substrate (Thermo Scientific, Waltham, MA, USA) on a ChemiDocTM MP imaging system (Bio-Rad, Hercules, CA, USA).

    Article Title: Orexin‐A Inhibits Lipopolysaccharide‐Induced Cell Migration in Cultured Mouse Astrocytes via Activation of Orexin 1 Receptor: Involvement of GABA Signaling
    Article Snippet: .. The membrane was incubated overnight at 4°C with a primary antibody specific for OXA (1:500, cat# AB3098, EMD Millipore), OX1R (1:500, cat#PA5‐77566, Invitrogen), GAT1 (1:300, cat# ab426, Abcam), GAT3 (1:300, cat# 25438, Cell Signaling Technology), KCC2 (mouse monoclonal anti‐KCC2 antibody, 1:500, cat# MA5‐27610, Thermo Fisher Scientific), phospho‐KCC2 (rabbit polyclonal anti‐phospho‐KCC2 (Thr‐1007) antibody, 1:500, cat# PA5‐95677, Thermo Fisher Scientific), ERK (1:1000, cat#9102, Cell Signaling Technology), phospho‐ERK (1:1000, cat#9101, Cell Signaling Technology), p38 MAPK (1:1000, cat#9212, Cell Signaling Technology), phospho‐p38 MAPK (1:1000, cat#9211, Cell Signaling Technology), or β‐actin (1:3000, cat#3700, Cell Signaling Technology). .. After three washes with TBST, the membrane was incubated for 1 h at room temperature with horseradish peroxidase (HRP)‐conjugated anti‐rabbit or anti‐mouse antibody (1:1000, Koma Biotech).

    Article Title: Docetaxel treatment upregulates estrogen receptor expression in triple negative breast cancer cells via activating arachidonic acid pathway
    Article Snippet: .. The membranes were blocked with 3% bovine serum albumin (BSA) to prevent nonspecific binding and incubated with primary antibodies: anti-Estrogen Receptor alpha antibody (ab75635, Abcam), Cleaved caspase 3 (9661, Cell Signaling Technology, CST), c-Jun (9165, CST), Phospho-c-Jun (3270, CST), Phospho-SAPK/JNK (4668, CST), Phospho-p38 MAPK (4511, CST), Phospho-p44/42 MAPK (Erk1/2, 4370, CST), and β-Actin antibody (4967, CST). .. After incubated with appropriate secondary antibodies, the bands were visualized using Clarity Western ECL Substrate (Bio-Rad) and imaged using a chemiluminescence detection system with auto-exposure setting.

    Electrophoresis:

    Article Title: Epigenetic Regulation of VCAM-1 by Lipoxin A4 Is Renoprotective Against Diabetic Kidney Disease
    Article Snippet: Cultured hGECs were lysed in M-PER Mammalian Protein Extraction Reagent (Thermo Fisher Scientific) with Phosphatase Inhibitor Cocktail 2 (Sigma) and Complete Protease Inhibitor Cocktail (Roche), and total protein was quantitated by bicinchoninic acid assay (Thermo Fisher Scientific). .. Following electrophoresis and transfer, the following primary antibodies were used: VCAM-1 (1:1,000; Abcam); phospho-p38 MAPK (1:200; Cell Signaling Technology [CST]); p38 MAPK (1:1,000; CST); phospho-nuclear factor-κB (NF-κB) p65 (1:200; CST); NF-κB p65 (1:1,000; CST); phospho-inhibitor of κBα (IκBα) (1:200; CST), IκBα (1:1,000; CST), and β-actin (1:20,000; Sigma-Aldrich), as previously described ( ). .. Antibodies for histone modifications included H3K4 monomethylation (H3K4me1) (cat. no. 07-436; Millipore), H3K27 acetylation (H3K27ac) (cat. no. ab4729; Abcam), H3K9 trimethylation (H3K9me3) (cat. no. ab8898; Abcam), and total H3 (cat. no. 14269 [1B1B2]; CST).

    Western Blot:

    Article Title: Bi-allelic EPHA2 mutations cause dysosteosclerosis by inhibiting osteoclastogenesis and enhancing osteoblastogenesis.
    Article Snippet: Immunohistochemistry staining was performed as described previously.48 The sections were incubated with rabbit anti-Osteocalcin antibodies (1:500; ab93876, Abcam) or anti-Sp7/ Osterix antibodies (1:500; ab209484, Abcam). .. Western blot analysis Protein extraction and western blot were performed as described previously.48 Each sample was probed for p38 MAPK (1:1 000 dilution, 9212, CST), phospho-p38 MAPK (Thr180/Tyr182) (1:1 000 dilution, 9211, CST) and β-tubulin (1:1 000 dilution, T40002, Abmart). ..

    Analysis:

    Article Title: Bi-allelic EPHA2 mutations cause dysosteosclerosis by inhibiting osteoclastogenesis and enhancing osteoblastogenesis.
    Article Snippet: Immunohistochemistry staining was performed as described previously.48 The sections were incubated with rabbit anti-Osteocalcin antibodies (1:500; ab93876, Abcam) or anti-Sp7/ Osterix antibodies (1:500; ab209484, Abcam). .. Western blot analysis Protein extraction and western blot were performed as described previously.48 Each sample was probed for p38 MAPK (1:1 000 dilution, 9212, CST), phospho-p38 MAPK (Thr180/Tyr182) (1:1 000 dilution, 9211, CST) and β-tubulin (1:1 000 dilution, T40002, Abmart). ..

    Protein Extraction:

    Article Title: Bi-allelic EPHA2 mutations cause dysosteosclerosis by inhibiting osteoclastogenesis and enhancing osteoblastogenesis.
    Article Snippet: Immunohistochemistry staining was performed as described previously.48 The sections were incubated with rabbit anti-Osteocalcin antibodies (1:500; ab93876, Abcam) or anti-Sp7/ Osterix antibodies (1:500; ab209484, Abcam). .. Western blot analysis Protein extraction and western blot were performed as described previously.48 Each sample was probed for p38 MAPK (1:1 000 dilution, 9212, CST), phospho-p38 MAPK (Thr180/Tyr182) (1:1 000 dilution, 9211, CST) and β-tubulin (1:1 000 dilution, T40002, Abmart). ..

    Membrane:

    Article Title: Orexin‐A Inhibits Lipopolysaccharide‐Induced Cell Migration in Cultured Mouse Astrocytes via Activation of Orexin 1 Receptor: Involvement of GABA Signaling
    Article Snippet: .. The membrane was incubated overnight at 4°C with a primary antibody specific for OXA (1:500, cat# AB3098, EMD Millipore), OX1R (1:500, cat#PA5‐77566, Invitrogen), GAT1 (1:300, cat# ab426, Abcam), GAT3 (1:300, cat# 25438, Cell Signaling Technology), KCC2 (mouse monoclonal anti‐KCC2 antibody, 1:500, cat# MA5‐27610, Thermo Fisher Scientific), phospho‐KCC2 (rabbit polyclonal anti‐phospho‐KCC2 (Thr‐1007) antibody, 1:500, cat# PA5‐95677, Thermo Fisher Scientific), ERK (1:1000, cat#9102, Cell Signaling Technology), phospho‐ERK (1:1000, cat#9101, Cell Signaling Technology), p38 MAPK (1:1000, cat#9212, Cell Signaling Technology), phospho‐p38 MAPK (1:1000, cat#9211, Cell Signaling Technology), or β‐actin (1:3000, cat#3700, Cell Signaling Technology). .. After three washes with TBST, the membrane was incubated for 1 h at room temperature with horseradish peroxidase (HRP)‐conjugated anti‐rabbit or anti‐mouse antibody (1:1000, Koma Biotech).

    other:

    Article Title: Hemoglobin inhibits fibroblast-to-cardiomyocyte reprogramming via TLR2/TLR4-dependent chromatin compaction
    Article Snippet: Band intensities were analyzed with either ImageJ or Syngene software.

    Hemagglutination Assay:

    Article Title: SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis
    Article Snippet: .. Primary antibodies used to specifically detect the proteins of interest were as follows: SIK2 (6919s, CST), GAPDH (G9545, Sigma-Aldrich), α-SMA (A5228, Sigma-Aldrich), Collagen I (AB765P, Sigma-Aldrich), Collagen III (AB7778, Abcam), CD31 (3528s, CST), Phospho-NF-κB P65 (Ser 536 ) (3033s, CST), NF-κB P65 (8242s, CST), Phospho-P38 MAPK (Thr 180 /Tyr 182 ) (4511s, CST), P38 MAPK (8690s, CST), α-Tubulin (66031-1, Proteintech), Histone H3 (68345-1, Proteintech), NOS2 (13120s, CST), FLAG-Tag (14793s, CST), HA-Tag (3724s, CST), TRAF1 (4710s, CST), TRAF2 (4724s, CST), TRAF4 (18527s, CST), TRAF6 (67591s, CST), His-Tag (12698s, CST), and Myc-Tag (2276s, CST). .. Anti-rabbit immunoglobulin G (IgG), horseradish peroxidase (HRP)–linked antibody (7074, CST) and anti-mouse IgG, HRP-linked antibody (7076, CST) were used to visualize the binding of primary antibodies in combination with the enhanced chemiluminescence (ECL) substrate.

    Nonspecific Binding:

    Article Title: Docetaxel treatment upregulates estrogen receptor expression in triple negative breast cancer cells via activating arachidonic acid pathway
    Article Snippet: .. The membranes were blocked with 3% bovine serum albumin (BSA) to prevent nonspecific binding and incubated with primary antibodies: anti-Estrogen Receptor alpha antibody (ab75635, Abcam), Cleaved caspase 3 (9661, Cell Signaling Technology, CST), c-Jun (9165, CST), Phospho-c-Jun (3270, CST), Phospho-SAPK/JNK (4668, CST), Phospho-p38 MAPK (4511, CST), Phospho-p44/42 MAPK (Erk1/2, 4370, CST), and β-Actin antibody (4967, CST). .. After incubated with appropriate secondary antibodies, the bands were visualized using Clarity Western ECL Substrate (Bio-Rad) and imaged using a chemiluminescence detection system with auto-exposure setting.

    Cell-Signaling:

    Article Title: Docetaxel treatment upregulates estrogen receptor expression in triple negative breast cancer cells via activating arachidonic acid pathway
    Article Snippet: .. The membranes were blocked with 3% bovine serum albumin (BSA) to prevent nonspecific binding and incubated with primary antibodies: anti-Estrogen Receptor alpha antibody (ab75635, Abcam), Cleaved caspase 3 (9661, Cell Signaling Technology, CST), c-Jun (9165, CST), Phospho-c-Jun (3270, CST), Phospho-SAPK/JNK (4668, CST), Phospho-p38 MAPK (4511, CST), Phospho-p44/42 MAPK (Erk1/2, 4370, CST), and β-Actin antibody (4967, CST). .. After incubated with appropriate secondary antibodies, the bands were visualized using Clarity Western ECL Substrate (Bio-Rad) and imaged using a chemiluminescence detection system with auto-exposure setting.



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    Image Search Results


    ( A ) KEGG enrichment analysis of down-regulated DEGs in Sik2 F/F ; LysM Cre cardiac macrophages on day 3 post-MI. The top 20 enriched pathways are listed. ( B ) DEGs (fold change ≥ 2 and P .adjust ≤ 0.05) overlapped in top 20 of enriched pathways. ( C ) Transcription factor prediction was performed using TRRUST databases. The top 10 transcription factors are listed. ( D ) Immunoblotting analysis and quantification of P65 in the cytoplasm and nucleus of WT and SIK2-knockout PMs and treated with TNF-α (20 ng/ml) or vehicle ( n = 4) for 1 hour. ( E ) qPCR analysis of Il-1β , Il-6 , Nos2 , Cxcl-1 , and Mmp-9 mRNA expression in WT and SIK2-knockout PMs stimulated with TNF-α for 24 hours ( n = 6). ( F ) qPCR analysis of Il-1β , Il-6 , Nos2 , Cxcl-1 , and Mmp-9 mRNA expression ( n = 6). PMs were pretreated with ARN3236 (3 μmol) and stimulated with TNF-α for 24 hours. ( G ) WikiPathways enrichment analysis of differentially phosphorylated proteins in PMs treated with ARN3236 (3 μmol) or control. The top 20 enriched pathways are listed. ( H ) Immunoblotting analysis and quantification of phosphorylated P65 (p-P65), P65, phosphorylated P38 (p-P38), and P38 expression in WT and SIK2-knockout PMs stimulated with TNF-α or vehicle ( n = 6). ( I and J ) Flow cytometry analysis of efferocytosis in WT or LeSik2 Raw264.7 cells [stimulated with SB 203580 (10 μmol) or not] treated with CFSE-prelabeled RBCs ( n = 6).

    Journal: Science Advances

    Article Title: SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis

    doi: 10.1126/sciadv.adw6624

    Figure Lengend Snippet: ( A ) KEGG enrichment analysis of down-regulated DEGs in Sik2 F/F ; LysM Cre cardiac macrophages on day 3 post-MI. The top 20 enriched pathways are listed. ( B ) DEGs (fold change ≥ 2 and P .adjust ≤ 0.05) overlapped in top 20 of enriched pathways. ( C ) Transcription factor prediction was performed using TRRUST databases. The top 10 transcription factors are listed. ( D ) Immunoblotting analysis and quantification of P65 in the cytoplasm and nucleus of WT and SIK2-knockout PMs and treated with TNF-α (20 ng/ml) or vehicle ( n = 4) for 1 hour. ( E ) qPCR analysis of Il-1β , Il-6 , Nos2 , Cxcl-1 , and Mmp-9 mRNA expression in WT and SIK2-knockout PMs stimulated with TNF-α for 24 hours ( n = 6). ( F ) qPCR analysis of Il-1β , Il-6 , Nos2 , Cxcl-1 , and Mmp-9 mRNA expression ( n = 6). PMs were pretreated with ARN3236 (3 μmol) and stimulated with TNF-α for 24 hours. ( G ) WikiPathways enrichment analysis of differentially phosphorylated proteins in PMs treated with ARN3236 (3 μmol) or control. The top 20 enriched pathways are listed. ( H ) Immunoblotting analysis and quantification of phosphorylated P65 (p-P65), P65, phosphorylated P38 (p-P38), and P38 expression in WT and SIK2-knockout PMs stimulated with TNF-α or vehicle ( n = 6). ( I and J ) Flow cytometry analysis of efferocytosis in WT or LeSik2 Raw264.7 cells [stimulated with SB 203580 (10 μmol) or not] treated with CFSE-prelabeled RBCs ( n = 6).

    Article Snippet: Primary antibodies used to specifically detect the proteins of interest were as follows: SIK2 (6919s, CST), GAPDH (G9545, Sigma-Aldrich), α-SMA (A5228, Sigma-Aldrich), Collagen I (AB765P, Sigma-Aldrich), Collagen III (AB7778, Abcam), CD31 (3528s, CST), Phospho-NF-κB P65 (Ser 536 ) (3033s, CST), NF-κB P65 (8242s, CST), Phospho-P38 MAPK (Thr 180 /Tyr 182 ) (4511s, CST), P38 MAPK (8690s, CST), α-Tubulin (66031-1, Proteintech), Histone H3 (68345-1, Proteintech), NOS2 (13120s, CST), FLAG-Tag (14793s, CST), HA-Tag (3724s, CST), TRAF1 (4710s, CST), TRAF2 (4724s, CST), TRAF4 (18527s, CST), TRAF6 (67591s, CST), His-Tag (12698s, CST), and Myc-Tag (2276s, CST).

    Techniques: Analysis, Western Blot, Knock-Out, Expressing, Control, Flow Cytometry, Significance Assay

    ( A ) Venn diagram delineating the intersection of SIK2-binding protein candidates in the top enriched pathways identified in , that is, NF-κB signaling pathway and MAPK signaling pathway. LC-MS/MS, liquid chromatography–tandem mass spectrometry. ( B ) Top proteins interacting with SIK2 identified through mass spectrometry analysis of peptides pulled down using anti-Flag antibody in HEK293T cells transfected with Flag-Sik2. ( C ) Immunoprecipitation in HEK293T cells transfected with Flag-Sik2 using anti-Flag antibody, followed by immunoblotting with corresponding antibodies. HA, hemagglutinin. ( D and E ) Immunoprecipitation in HEK293T cells transfected with Flag-Sik2 and HA-Traf2 using anti-Flag (D) or anti-HA (E) antibody, followed by immunoblotting with corresponding antibodies. FL, full length. ( F ) Immunoprecipitation (IP) in HEK293T cells cotransfected with HA-Traf2 and truncated Flag-Sik2 using an anti-HA antibody, followed by immunoblotting (IB) with corresponding antibodies. ( G ) Immunoprecipitation in HEK293T cells cotransfected with Flag-Sik2 and truncated HA-Traf2 using an anti-HA antibody, followed by immunoblotting with corresponding antibodies. ( H ) Western blotting analysis and quantification of SIK2, TRAF2, p-P38, P38, p-P65, and P65 expression in HEK293T cells transfected with SIK2 and si-TRAF2 or control ( n = 4). ( I ) Coimmunoprecipitation (Co-IP) analysis of TRAF2 ubiquitination in HEK293T cells cotransfected with HA-Traf2 and His-Ub, along with Flag-Sik2 or Flag-Sik2 T175A mutant. ( J ) Co-IP analysis of TRAF2 ubiquitination in HEK293T cells cotransfected with HA-Traf2 and Flag-Sik2, along with Myc-K48-Ub or Myc-K63-Ub. ( K ) Co-IP analysis of TRAF2 phosphate serine (p-Ser) and phosphate threonine (p-Thr) in HEK293T cells transfected with HA-Traf2, along with Flag-Sik2 or Flag-Sik2 T175A mutant.

    Journal: Science Advances

    Article Title: SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis

    doi: 10.1126/sciadv.adw6624

    Figure Lengend Snippet: ( A ) Venn diagram delineating the intersection of SIK2-binding protein candidates in the top enriched pathways identified in , that is, NF-κB signaling pathway and MAPK signaling pathway. LC-MS/MS, liquid chromatography–tandem mass spectrometry. ( B ) Top proteins interacting with SIK2 identified through mass spectrometry analysis of peptides pulled down using anti-Flag antibody in HEK293T cells transfected with Flag-Sik2. ( C ) Immunoprecipitation in HEK293T cells transfected with Flag-Sik2 using anti-Flag antibody, followed by immunoblotting with corresponding antibodies. HA, hemagglutinin. ( D and E ) Immunoprecipitation in HEK293T cells transfected with Flag-Sik2 and HA-Traf2 using anti-Flag (D) or anti-HA (E) antibody, followed by immunoblotting with corresponding antibodies. FL, full length. ( F ) Immunoprecipitation (IP) in HEK293T cells cotransfected with HA-Traf2 and truncated Flag-Sik2 using an anti-HA antibody, followed by immunoblotting (IB) with corresponding antibodies. ( G ) Immunoprecipitation in HEK293T cells cotransfected with Flag-Sik2 and truncated HA-Traf2 using an anti-HA antibody, followed by immunoblotting with corresponding antibodies. ( H ) Western blotting analysis and quantification of SIK2, TRAF2, p-P38, P38, p-P65, and P65 expression in HEK293T cells transfected with SIK2 and si-TRAF2 or control ( n = 4). ( I ) Coimmunoprecipitation (Co-IP) analysis of TRAF2 ubiquitination in HEK293T cells cotransfected with HA-Traf2 and His-Ub, along with Flag-Sik2 or Flag-Sik2 T175A mutant. ( J ) Co-IP analysis of TRAF2 ubiquitination in HEK293T cells cotransfected with HA-Traf2 and Flag-Sik2, along with Myc-K48-Ub or Myc-K63-Ub. ( K ) Co-IP analysis of TRAF2 phosphate serine (p-Ser) and phosphate threonine (p-Thr) in HEK293T cells transfected with HA-Traf2, along with Flag-Sik2 or Flag-Sik2 T175A mutant.

    Article Snippet: Primary antibodies used to specifically detect the proteins of interest were as follows: SIK2 (6919s, CST), GAPDH (G9545, Sigma-Aldrich), α-SMA (A5228, Sigma-Aldrich), Collagen I (AB765P, Sigma-Aldrich), Collagen III (AB7778, Abcam), CD31 (3528s, CST), Phospho-NF-κB P65 (Ser 536 ) (3033s, CST), NF-κB P65 (8242s, CST), Phospho-P38 MAPK (Thr 180 /Tyr 182 ) (4511s, CST), P38 MAPK (8690s, CST), α-Tubulin (66031-1, Proteintech), Histone H3 (68345-1, Proteintech), NOS2 (13120s, CST), FLAG-Tag (14793s, CST), HA-Tag (3724s, CST), TRAF1 (4710s, CST), TRAF2 (4724s, CST), TRAF4 (18527s, CST), TRAF6 (67591s, CST), His-Tag (12698s, CST), and Myc-Tag (2276s, CST).

    Techniques: Binding Assay, Liquid Chromatography with Mass Spectroscopy, Liquid Chromatography, Mass Spectrometry, Analysis, Transfection, Immunoprecipitation, Western Blot, Expressing, Control, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Mutagenesis, Tandem Mass Spectroscopy

    ( A ) Experimental design depicting AAV and P38 inhibitor SB 203580 injection in mice before or after MI. ip, intraperitoneally. ( B ) Immunoblotting analysis and quantification of SIK2 in infarct macrophages from AAV.F4/80.SIK2 or AAV.F4/80.NC injected mice ( n = 4 for AAV.F4/80.NC; n = 6 for AAV.F4/80.SIK2). ( C ) Representative parasternal long-axis views and M-mode images are shown. Summarized data of echocardiographic measurements in WT mice administrated with AAV.F4/80.SIK2 or AAV.F4/80.NC treated with SB 203580 or vehicle ( n = 6). ( D ) Masson’s trichrome staining for infarct size measurements in designated groups at day 14 after MI ( n = 6). ( E ) Representative parasternal long-axis views and M-mode images are shown. ( F and G ) Summarized data of echocardiographic measurements in WT mice administrated with AAV.F4/80.SIK2 T175A or AAV.F4/80.NC ( n = 6). ( H ) Masson’s trichrome staining for infarct measurements in designated groups at day 14 after MI ( n = 6).

    Journal: Science Advances

    Article Title: SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis

    doi: 10.1126/sciadv.adw6624

    Figure Lengend Snippet: ( A ) Experimental design depicting AAV and P38 inhibitor SB 203580 injection in mice before or after MI. ip, intraperitoneally. ( B ) Immunoblotting analysis and quantification of SIK2 in infarct macrophages from AAV.F4/80.SIK2 or AAV.F4/80.NC injected mice ( n = 4 for AAV.F4/80.NC; n = 6 for AAV.F4/80.SIK2). ( C ) Representative parasternal long-axis views and M-mode images are shown. Summarized data of echocardiographic measurements in WT mice administrated with AAV.F4/80.SIK2 or AAV.F4/80.NC treated with SB 203580 or vehicle ( n = 6). ( D ) Masson’s trichrome staining for infarct size measurements in designated groups at day 14 after MI ( n = 6). ( E ) Representative parasternal long-axis views and M-mode images are shown. ( F and G ) Summarized data of echocardiographic measurements in WT mice administrated with AAV.F4/80.SIK2 T175A or AAV.F4/80.NC ( n = 6). ( H ) Masson’s trichrome staining for infarct measurements in designated groups at day 14 after MI ( n = 6).

    Article Snippet: Primary antibodies used to specifically detect the proteins of interest were as follows: SIK2 (6919s, CST), GAPDH (G9545, Sigma-Aldrich), α-SMA (A5228, Sigma-Aldrich), Collagen I (AB765P, Sigma-Aldrich), Collagen III (AB7778, Abcam), CD31 (3528s, CST), Phospho-NF-κB P65 (Ser 536 ) (3033s, CST), NF-κB P65 (8242s, CST), Phospho-P38 MAPK (Thr 180 /Tyr 182 ) (4511s, CST), P38 MAPK (8690s, CST), α-Tubulin (66031-1, Proteintech), Histone H3 (68345-1, Proteintech), NOS2 (13120s, CST), FLAG-Tag (14793s, CST), HA-Tag (3724s, CST), TRAF1 (4710s, CST), TRAF2 (4724s, CST), TRAF4 (18527s, CST), TRAF6 (67591s, CST), His-Tag (12698s, CST), and Myc-Tag (2276s, CST).

    Techniques: Injection, Western Blot, Analysis, Staining