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rabbit monoclonal anti p38 mitogen-activated protein (map) kinase  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc rabbit monoclonal anti p38 mitogen-activated protein (map) kinase
    Rabbit Monoclonal Anti P38 Mitogen Activated Protein (Map) Kinase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 817 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p38+map+kinase+activity/Phospho-p38+MAPK+(Thr180%2FTyr182)+Rabbit+mAb/pm38999828-46-7-51
    Average 96 stars, based on 817 article reviews
    rabbit monoclonal anti p38 mitogen-activated protein (map) kinase - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Activity Assay:

    Article Title: Dual Function of PPARγ in CD11c+ Cells Ensures Immune Tolerance in the Airways
    Article Snippet: .. p38 MAP kinase activity in cell extracts was performed using a non-radioactive p38 MAP kinase assay kit (Cell Signaling) following manufacturer’s instructions. .. Student’s unpaired two-tailed t-test and one-way ANOVA with Tukey’s post hoc test was performed wherever applicable, using GraphPad Prism 5.

    Article Title: A Novel Chromone Derivative with Anti-Inflammatory Property via Inhibition of ROS-Dependent Activation of TRAF6-ASK1-p38 Pathway
    Article Snippet: .. Cells were stimulated by 500 ng/ml LPS for 6 h and the protein was collected. p38 MAP Kinase activity was detected by p38 MAP Kinase Assay Kit (Cell Signaling Technology). ..

    Article Title: PSM/SH2-B distributes selected mitogenic receptor signals to distinct components in the PI3-kinase and MAP kinase signaling pathways.
    Article Snippet: The Pro-rich, PH, and SH2 domain containing mitogenic signaling adapter PSM/SH2-B has been implicated as a cellular partner of variousmitogenic receptor tyrosine kinases and related signalingmechanisms.Here,we report in a direct comparison of three peptide hormones, that PSM participates in the assembly of distinct mitogenic signaling complexes in response to insulin or IGF-I when compared to PDGF in cultured normal fibroblasts.. The complex formed in response to insulin or IGF-I involves the respective peptide hormone receptor and presumably the established components leading to MAP kinase activation.. However, our data suggest an alternative link from the PDGF receptor via PSM directly toMEK1/2 and consequently also to p44/42 activation, possibly through a scaffold protein.

    Article Title: ? 1 -Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional Regulation: Involvement of p38 Mitogen-Activated Protein Kinase and Nuclear Factor-?B
    Article Snippet: After removal of blotting solution containing primary antibody, the blot was incubated with a horseradish peroxidase-conjugated secondary antibody at room temperature for 1 h, and the signal was detected by chemiluminescence (Pierce, Rockford, IL). p38 Kinase Activity Assay. .. The Nonradioactive p38 MAP Kinase Assay Kit from Cell Signaling Technology was used to determine p38 MAP kinase activity by measuring phosphorylated ATF-2. ..

    Article Title: S. aureus haemolysin A-induced IL-8 and IL-6 release from human airway epithelial cells is mediated by activation of p38- and Erk-MAP kinases and additional, cell type-specific signalling mechanisms.
    Article Snippet: .. Antibodies against phosphorylated and non-phosphorylated forms of p38 MAP kinase as well as the non-radioactive assay kit for measuring p38 MAP kinase activity were obtained from Cell Signaling Technology and purchased through NEB (Frankfurt, Germany). .. Molecular mass marker proteins and b-actin antibodies (A1978) were obtained from Sigma-Aldrich (Munich, Germany).

    Article Title: Exposure of airway epithelium to bile acids associated with gastroesophageal reflux symptoms: a relation to transforming growth factor-beta1 production and fibroblast proliferation.
    Article Snippet: Rationale: Gastroesophageal reflux (GER) is common in patients with various airway diseases.. Airway epithelial cells can release growth factors that promote fibroblast proliferation.. Exposure of airway epithelium to bile acids may induce a fibrotic response.

    Article Title: 15-deoxy-delta 12,14-prostaglandin J(2) inhibits the synthesis of the acute phase protein SIP24 in cartilage: Involvement of COX-2 in resolution of inflammation.
    Article Snippet: Cellular Physiology 15-Deoxy-Delta12, 14-Prostaglandin J2 Inhibits the Synthesis of the Acute Phase Protein SIP24 in Cartilage: Involvement of COX-2 in Resolution of Inflammation VALENTINA ULIVI, RANIERI CANCEDDA, AND FIORELLA DESCALZI CANCEDDA* Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy Dipartimento di Oncologia, Biologia e Genetica, Universita’ di Genova, Genova, Italy Istituto Bioimmagini e Fisiologia Molecolare, Consiglio Nazionale delle Ricerche, Sezione di Genova, Genova, Italy

    Article Title: Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.
    Article Snippet: Sumida, Tomohiko, Hajime Otani, Shiori Kyoi, Takayuki Okada, Hiroyoshi Fujiwara, Yoshihisa Nakao, Masakuni Kido, and Hiroji Imamura.. Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.. Am J Physiol Heart Circ Physiol 288: H2726–H2734, 2005.

    Kinase Assay:

    Article Title: Dual Function of PPARγ in CD11c+ Cells Ensures Immune Tolerance in the Airways
    Article Snippet: .. p38 MAP kinase activity in cell extracts was performed using a non-radioactive p38 MAP kinase assay kit (Cell Signaling) following manufacturer’s instructions. .. Student’s unpaired two-tailed t-test and one-way ANOVA with Tukey’s post hoc test was performed wherever applicable, using GraphPad Prism 5.

    Article Title: A Novel Chromone Derivative with Anti-Inflammatory Property via Inhibition of ROS-Dependent Activation of TRAF6-ASK1-p38 Pathway
    Article Snippet: .. Cells were stimulated by 500 ng/ml LPS for 6 h and the protein was collected. p38 MAP Kinase activity was detected by p38 MAP Kinase Assay Kit (Cell Signaling Technology). ..

    Article Title: PSM/SH2-B distributes selected mitogenic receptor signals to distinct components in the PI3-kinase and MAP kinase signaling pathways.
    Article Snippet: The Pro-rich, PH, and SH2 domain containing mitogenic signaling adapter PSM/SH2-B has been implicated as a cellular partner of variousmitogenic receptor tyrosine kinases and related signalingmechanisms.Here,we report in a direct comparison of three peptide hormones, that PSM participates in the assembly of distinct mitogenic signaling complexes in response to insulin or IGF-I when compared to PDGF in cultured normal fibroblasts.. The complex formed in response to insulin or IGF-I involves the respective peptide hormone receptor and presumably the established components leading to MAP kinase activation.. However, our data suggest an alternative link from the PDGF receptor via PSM directly toMEK1/2 and consequently also to p44/42 activation, possibly through a scaffold protein.

    Article Title: ? 1 -Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional Regulation: Involvement of p38 Mitogen-Activated Protein Kinase and Nuclear Factor-?B
    Article Snippet: After removal of blotting solution containing primary antibody, the blot was incubated with a horseradish peroxidase-conjugated secondary antibody at room temperature for 1 h, and the signal was detected by chemiluminescence (Pierce, Rockford, IL). p38 Kinase Activity Assay. .. The Nonradioactive p38 MAP Kinase Assay Kit from Cell Signaling Technology was used to determine p38 MAP kinase activity by measuring phosphorylated ATF-2. ..

    Article Title: 15-deoxy-delta 12,14-prostaglandin J(2) inhibits the synthesis of the acute phase protein SIP24 in cartilage: Involvement of COX-2 in resolution of inflammation.
    Article Snippet: Cellular Physiology 15-Deoxy-Delta12, 14-Prostaglandin J2 Inhibits the Synthesis of the Acute Phase Protein SIP24 in Cartilage: Involvement of COX-2 in Resolution of Inflammation VALENTINA ULIVI, RANIERI CANCEDDA, AND FIORELLA DESCALZI CANCEDDA* Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy Dipartimento di Oncologia, Biologia e Genetica, Universita’ di Genova, Genova, Italy Istituto Bioimmagini e Fisiologia Molecolare, Consiglio Nazionale delle Ricerche, Sezione di Genova, Genova, Italy

    Article Title: Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.
    Article Snippet: Sumida, Tomohiko, Hajime Otani, Shiori Kyoi, Takayuki Okada, Hiroyoshi Fujiwara, Yoshihisa Nakao, Masakuni Kido, and Hiroji Imamura.. Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.. Am J Physiol Heart Circ Physiol 288: H2726–H2734, 2005.

    Western Blot:

    Article Title: PSM/SH2-B distributes selected mitogenic receptor signals to distinct components in the PI3-kinase and MAP kinase signaling pathways.
    Article Snippet: The Pro-rich, PH, and SH2 domain containing mitogenic signaling adapter PSM/SH2-B has been implicated as a cellular partner of variousmitogenic receptor tyrosine kinases and related signalingmechanisms.Here,we report in a direct comparison of three peptide hormones, that PSM participates in the assembly of distinct mitogenic signaling complexes in response to insulin or IGF-I when compared to PDGF in cultured normal fibroblasts.. The complex formed in response to insulin or IGF-I involves the respective peptide hormone receptor and presumably the established components leading to MAP kinase activation.. However, our data suggest an alternative link from the PDGF receptor via PSM directly toMEK1/2 and consequently also to p44/42 activation, possibly through a scaffold protein.



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    Alleviation of cynaropicrin-induced cytotoxicity through a <t>p38</t> <t>MAPK</t> inhibitor in Hep3B cells. (A) After treating cells with cynaropicrin for the indicated duration, changes in the expression of the three types of MAPKs were examined via Western blot analysis. (B-D) Cells were pretreated with the p38 MAPK inhibitor SB203580 for 1 h and then treated with cynaropicrin for 24 h. Thereafter, changes in morphology (B), cell viability (C), and expression of the indicated proteins (D) were examined. (C) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; ### p <0.001 compared to cynaropicrin-treated group.
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    Alleviation of cynaropicrin-induced cytotoxicity through a <t>p38</t> <t>MAPK</t> inhibitor in Hep3B cells. (A) After treating cells with cynaropicrin for the indicated duration, changes in the expression of the three types of MAPKs were examined via Western blot analysis. (B-D) Cells were pretreated with the p38 MAPK inhibitor SB203580 for 1 h and then treated with cynaropicrin for 24 h. Thereafter, changes in morphology (B), cell viability (C), and expression of the indicated proteins (D) were examined. (C) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; ### p <0.001 compared to cynaropicrin-treated group.
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    Figure 4. CD147-K148me2 facilitates CCL5 secretion in NSCLC cells by activating <t>CyPA-CD147-p38</t> signaling. A) Temperature factor (B-factor) distri- bution and K148 location of the CD147 molecule (PDB ID: 3B5H). B-factor values range from blue (low B-factor) to red (high B-factor). B) Structural superposition of CD147 (gray) and CD147-K148me2 (orange) based on their respective complex docking models. Arrows indicate local conformational changes induced by di-methylation, and yellow dashed lines indicate polar contacts formed between amino acid residues. C) Close-up view of the inter- action interfaces of the docked complex model between CyPA (pink) and CD147 (green) without (upper) or with (lower) K148me2. K148 (red) and amino
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    Cell Signaling Technology Inc phospho specific p38 mitogen activated protein map kinase antibodies
    Phosphorylated <t>p38</t> mitogen-activated protein kinase in the platelets and the levels of phosphorylated Akt corrected with those of phosphorylated p38 mitogen-activated protein kinase. A and B: Type 2 diabetes mellitus (T2DM) group; C and D: The control group. To avoid platelet activation, ice-cold ethylenediaminetetraacetic acid (10 mmol/L) solution was added immediately to the platelet-rich plasma obtained from patients in the T2DM group (A and B) and the control group (C and D). The lysates of the platelets were then subjected to western blot analysis using antibodies against phospho-specific p38 Mitogen-activated protein kinase <t>(MAPK).</t> All the results are presented collectively (A: n = 40; C: n = 15). The levels of phosphorylated-p38 MAPK were determined using the ImageJ software program. The bar graphs show the levels of phosphorylated-Akt corrected with those of phosphorylated p38 MAPK in the T2DM group (B) and the control group (D). MAPK: Mitogen-activated protein kinase.
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    Cell Signaling Technology Inc phospho p38 mitogen activated protein map kinase
    Phosphorylated <t>p38</t> mitogen-activated protein kinase in the platelets and the levels of phosphorylated Akt corrected with those of phosphorylated p38 mitogen-activated protein kinase. A and B: Type 2 diabetes mellitus (T2DM) group; C and D: The control group. To avoid platelet activation, ice-cold ethylenediaminetetraacetic acid (10 mmol/L) solution was added immediately to the platelet-rich plasma obtained from patients in the T2DM group (A and B) and the control group (C and D). The lysates of the platelets were then subjected to western blot analysis using antibodies against phospho-specific p38 Mitogen-activated protein kinase <t>(MAPK).</t> All the results are presented collectively (A: n = 40; C: n = 15). The levels of phosphorylated-p38 MAPK were determined using the ImageJ software program. The bar graphs show the levels of phosphorylated-Akt corrected with those of phosphorylated p38 MAPK in the T2DM group (B) and the control group (D). MAPK: Mitogen-activated protein kinase.
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    Image Search Results


    Alleviation of cynaropicrin-induced cytotoxicity through a p38 MAPK inhibitor in Hep3B cells. (A) After treating cells with cynaropicrin for the indicated duration, changes in the expression of the three types of MAPKs were examined via Western blot analysis. (B-D) Cells were pretreated with the p38 MAPK inhibitor SB203580 for 1 h and then treated with cynaropicrin for 24 h. Thereafter, changes in morphology (B), cell viability (C), and expression of the indicated proteins (D) were examined. (C) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; ### p <0.001 compared to cynaropicrin-treated group.

    Journal: Biomolecules & Therapeutics

    Article Title: Cynaropicrin Induces Reactive Oxygen Species-Dependent Paraptosis-Like Cell Death in Human Liver Cancer Cells

    doi: 10.4062/biomolther.2025.011

    Figure Lengend Snippet: Alleviation of cynaropicrin-induced cytotoxicity through a p38 MAPK inhibitor in Hep3B cells. (A) After treating cells with cynaropicrin for the indicated duration, changes in the expression of the three types of MAPKs were examined via Western blot analysis. (B-D) Cells were pretreated with the p38 MAPK inhibitor SB203580 for 1 h and then treated with cynaropicrin for 24 h. Thereafter, changes in morphology (B), cell viability (C), and expression of the indicated proteins (D) were examined. (C) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; ### p <0.001 compared to cynaropicrin-treated group.

    Article Snippet: Antibodies against poly(ADP-ribose) polymerase (PARP), apoptosis-linked gene 2-interacting protein X (Alix), p38 mitogen activated protein kinase (MAPK), extracellular signal-regulated kinase ( de Ridder et al ., 2023 ), c-Jun N-terminal kinases (JNK), phosphor (p)-JNK, and β-actin were purchased from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, USA).

    Techniques: Expressing, Western Blot

    Effects of the p38 MAPK inhibitor on cynaropicrin-induced ER stress and mitochondrial impairment in Hep3B cells. The effects of SB203580 on the cynaropicrin-induced increase in intracellular Ca 2+ concentration (A, B), ER stress (C, D), and mitochondrial dysfunction (E, F) were evaluated via flow cytometry. (B, D, F) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; # p <0.05 and ### p <0.001 compared to cynaropicrin-treated group.

    Journal: Biomolecules & Therapeutics

    Article Title: Cynaropicrin Induces Reactive Oxygen Species-Dependent Paraptosis-Like Cell Death in Human Liver Cancer Cells

    doi: 10.4062/biomolther.2025.011

    Figure Lengend Snippet: Effects of the p38 MAPK inhibitor on cynaropicrin-induced ER stress and mitochondrial impairment in Hep3B cells. The effects of SB203580 on the cynaropicrin-induced increase in intracellular Ca 2+ concentration (A, B), ER stress (C, D), and mitochondrial dysfunction (E, F) were evaluated via flow cytometry. (B, D, F) Numerical data are presented as mean ± SD (n=3). *** p <0.001 compared to untreated group; # p <0.05 and ### p <0.001 compared to cynaropicrin-treated group.

    Article Snippet: Antibodies against poly(ADP-ribose) polymerase (PARP), apoptosis-linked gene 2-interacting protein X (Alix), p38 mitogen activated protein kinase (MAPK), extracellular signal-regulated kinase ( de Ridder et al ., 2023 ), c-Jun N-terminal kinases (JNK), phosphor (p)-JNK, and β-actin were purchased from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, USA).

    Techniques: Concentration Assay, Flow Cytometry

    A schematic diagram illustrating the mechanisms by which cynaropicrin induces cell death in Hep3B cells, including the promotion of mitochondrial ROS production, activation of the p38 MAPK pathway, inhibition of Alix protein, and enhancement of ER stress.

    Journal: Biomolecules & Therapeutics

    Article Title: Cynaropicrin Induces Reactive Oxygen Species-Dependent Paraptosis-Like Cell Death in Human Liver Cancer Cells

    doi: 10.4062/biomolther.2025.011

    Figure Lengend Snippet: A schematic diagram illustrating the mechanisms by which cynaropicrin induces cell death in Hep3B cells, including the promotion of mitochondrial ROS production, activation of the p38 MAPK pathway, inhibition of Alix protein, and enhancement of ER stress.

    Article Snippet: Antibodies against poly(ADP-ribose) polymerase (PARP), apoptosis-linked gene 2-interacting protein X (Alix), p38 mitogen activated protein kinase (MAPK), extracellular signal-regulated kinase ( de Ridder et al ., 2023 ), c-Jun N-terminal kinases (JNK), phosphor (p)-JNK, and β-actin were purchased from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, USA).

    Techniques: Activation Assay, Inhibition

    Figure 4. CD147-K148me2 facilitates CCL5 secretion in NSCLC cells by activating CyPA-CD147-p38 signaling. A) Temperature factor (B-factor) distri- bution and K148 location of the CD147 molecule (PDB ID: 3B5H). B-factor values range from blue (low B-factor) to red (high B-factor). B) Structural superposition of CD147 (gray) and CD147-K148me2 (orange) based on their respective complex docking models. Arrows indicate local conformational changes induced by di-methylation, and yellow dashed lines indicate polar contacts formed between amino acid residues. C) Close-up view of the inter- action interfaces of the docked complex model between CyPA (pink) and CD147 (green) without (upper) or with (lower) K148me2. K148 (red) and amino

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: CD147-K148me2-Driven Tumor Cell-Macrophage Crosstalk Provokes NSCLC Immunosuppression via the CCL5/CCR5 Axis.

    doi: 10.1002/advs.202400611

    Figure Lengend Snippet: Figure 4. CD147-K148me2 facilitates CCL5 secretion in NSCLC cells by activating CyPA-CD147-p38 signaling. A) Temperature factor (B-factor) distri- bution and K148 location of the CD147 molecule (PDB ID: 3B5H). B-factor values range from blue (low B-factor) to red (high B-factor). B) Structural superposition of CD147 (gray) and CD147-K148me2 (orange) based on their respective complex docking models. Arrows indicate local conformational changes induced by di-methylation, and yellow dashed lines indicate polar contacts formed between amino acid residues. C) Close-up view of the inter- action interfaces of the docked complex model between CyPA (pink) and CD147 (green) without (upper) or with (lower) K148me2. K148 (red) and amino

    Article Snippet: U-46619 (HY-108566, MCE, 10 μM) was utilized as a p38 MAPK activator, while Maraviroc (HY-13004, MCE, 100 nM) was used as a CCR5 inhibitor in this study.

    Techniques: Methylation

    Phosphorylated p38 mitogen-activated protein kinase in the platelets and the levels of phosphorylated Akt corrected with those of phosphorylated p38 mitogen-activated protein kinase. A and B: Type 2 diabetes mellitus (T2DM) group; C and D: The control group. To avoid platelet activation, ice-cold ethylenediaminetetraacetic acid (10 mmol/L) solution was added immediately to the platelet-rich plasma obtained from patients in the T2DM group (A and B) and the control group (C and D). The lysates of the platelets were then subjected to western blot analysis using antibodies against phospho-specific p38 Mitogen-activated protein kinase (MAPK). All the results are presented collectively (A: n = 40; C: n = 15). The levels of phosphorylated-p38 MAPK were determined using the ImageJ software program. The bar graphs show the levels of phosphorylated-Akt corrected with those of phosphorylated p38 MAPK in the T2DM group (B) and the control group (D). MAPK: Mitogen-activated protein kinase.

    Journal: World Journal of Clinical Cases

    Article Title: Inverse relationship between platelet Akt activity and hippocampal atrophy: A pilot case-control study in patients with diabetes mellitus

    doi: 10.12998/wjcc.v12.i2.302

    Figure Lengend Snippet: Phosphorylated p38 mitogen-activated protein kinase in the platelets and the levels of phosphorylated Akt corrected with those of phosphorylated p38 mitogen-activated protein kinase. A and B: Type 2 diabetes mellitus (T2DM) group; C and D: The control group. To avoid platelet activation, ice-cold ethylenediaminetetraacetic acid (10 mmol/L) solution was added immediately to the platelet-rich plasma obtained from patients in the T2DM group (A and B) and the control group (C and D). The lysates of the platelets were then subjected to western blot analysis using antibodies against phospho-specific p38 Mitogen-activated protein kinase (MAPK). All the results are presented collectively (A: n = 40; C: n = 15). The levels of phosphorylated-p38 MAPK were determined using the ImageJ software program. The bar graphs show the levels of phosphorylated-Akt corrected with those of phosphorylated p38 MAPK in the T2DM group (B) and the control group (D). MAPK: Mitogen-activated protein kinase.

    Article Snippet: Phospho-specific Akt (Thr-308) and phospho-specific p38 mitogen-activated protein (MAP) kinase antibodies were purchased from Cell Signaling Technology, Inc. (Danvers, MA).

    Techniques: Control, Activation Assay, Clinical Proteomics, Western Blot, Software

    The relationship between the individual levels of phosphorylated Akt corrected with phosphorylated p38 mitogen-activated protein kinase (phosphorylated Akt/phosphorylated p38 mitogen-activated protein kinase) and the voxel-based specific regional analysis system for Alzheimer’s disease Z-score. A: Type 2 diabetes mellitus (T2DM) group; B: The control group. The levels of phosphorylated Akt corrected with phosphorylated-p38 mitogen-activated protein kinase (MAPK) (phosphorylated-Akt/phosphorylated-p38 MAPK) in the T2DM group (A) and the control group (B) were plotted against the voxel-based specific regional analysis system for Alzheimer’s disease Z-scores. The plotted data were analysed by linear regression analysis. VSRAD: Voxel-based specific regional analysis system for Alzheimer’s disease; MAPK: Mitogen-activated protein kinase.

    Journal: World Journal of Clinical Cases

    Article Title: Inverse relationship between platelet Akt activity and hippocampal atrophy: A pilot case-control study in patients with diabetes mellitus

    doi: 10.12998/wjcc.v12.i2.302

    Figure Lengend Snippet: The relationship between the individual levels of phosphorylated Akt corrected with phosphorylated p38 mitogen-activated protein kinase (phosphorylated Akt/phosphorylated p38 mitogen-activated protein kinase) and the voxel-based specific regional analysis system for Alzheimer’s disease Z-score. A: Type 2 diabetes mellitus (T2DM) group; B: The control group. The levels of phosphorylated Akt corrected with phosphorylated-p38 mitogen-activated protein kinase (MAPK) (phosphorylated-Akt/phosphorylated-p38 MAPK) in the T2DM group (A) and the control group (B) were plotted against the voxel-based specific regional analysis system for Alzheimer’s disease Z-scores. The plotted data were analysed by linear regression analysis. VSRAD: Voxel-based specific regional analysis system for Alzheimer’s disease; MAPK: Mitogen-activated protein kinase.

    Article Snippet: Phospho-specific Akt (Thr-308) and phospho-specific p38 mitogen-activated protein (MAP) kinase antibodies were purchased from Cell Signaling Technology, Inc. (Danvers, MA).

    Techniques: Control