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primary antibody p p38 mapk rabbit mab  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc primary antibody p p38 mapk rabbit mab
    Primary Antibody P P38 Mapk Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibody p p38 mapk rabbit mab/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    primary antibody p p38 mapk rabbit mab - by Bioz Stars, 2025-01
    86/100 stars

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    Cell Signaling Technology Inc rabbit anti p p38 mapk
    IL-33 Inhibits the expression of tight junction proteins in BMEC and enhances activation of the <t>p38</t> signaling pathway. ( A ) IL-33 suppresses the expression of Claudin-5 and can cause abnormal distribution of Claudin-5. ( B ) Relative protein expression of Claudin-5. ( C ) Immunofluorescence analysis method is used to examine the expression and distribution of Claudin-5 in hCMEC/D3 due to IL-33. The working concentration of IL-33 is 10 ng/mL. Bar, 10 µM. ( D ) IL-33 promotes the expression of MMP-9 and phosphorylation of p38 in hCMEC/D3. ( E ) Grayscale analysis of the expression of MMP-9. ( F ) Grayscale analysis of the expression of p38, and phosphorylated p38. ( G ) MMP-9 expression in cells treatment with IL-33 was measured using ELISA ( n = 3). The data are presented as the mean ± standard deviation (SD) and were analyzed by one-way ANOVA. ** P < 0.01, * P < 0.05.
    Rabbit Anti P P38 Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc rabbit polyclonal anti p p38 mapk
    Evidence that <t>p38</t> is critical for CPC-induced paraptosis (A) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC for 24 h. (B and C) Cytotoxicity of MIAPaCa2 and SW1990 cells treated with CPC in the absence or presence of the GS4997 (10 μM) or doramapimod (5 μM) for 24 h. (D) MIAPaCa2 and SW1990 cells were treated with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h. ER structures were stained with ER-Tracker Red. Scale bar: 10 μm. (E) Light microscopy analysis of cell morphology in indicated MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h, followed by quantitative assessment. (F–H) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of tauroursodeoxycholate (TUDC; 1 mM), 4μ8C (100 μM), or GS4997 (10 μM) for 24 h. Data are presented as mean ± SD. The proportion of cells displaying vacuoles was determined by visually examining a minimum of 100 cells, and the data are presented as the mean ± SD from at least three independent experiments (E). p values were calculated by one-way ANOVA (A, E, F, G, and H) or two-way ANOVA (B and C). See also <xref ref-type=Figure S4 . " width="250" height="auto" />
    Rabbit Polyclonal Anti P P38 Mapk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology rabbit poab anti p p38 mapk
    Evidence that <t>p38</t> is critical for CPC-induced paraptosis (A) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC for 24 h. (B and C) Cytotoxicity of MIAPaCa2 and SW1990 cells treated with CPC in the absence or presence of the GS4997 (10 μM) or doramapimod (5 μM) for 24 h. (D) MIAPaCa2 and SW1990 cells were treated with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h. ER structures were stained with ER-Tracker Red. Scale bar: 10 μm. (E) Light microscopy analysis of cell morphology in indicated MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h, followed by quantitative assessment. (F–H) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of tauroursodeoxycholate (TUDC; 1 mM), 4μ8C (100 μM), or GS4997 (10 μM) for 24 h. Data are presented as mean ± SD. The proportion of cells displaying vacuoles was determined by visually examining a minimum of 100 cells, and the data are presented as the mean ± SD from at least three independent experiments (E). p values were calculated by one-way ANOVA (A, E, F, G, and H) or two-way ANOVA (B and C). See also <xref ref-type=Figure S4 . " width="250" height="auto" />
    Rabbit Poab Anti P P38 Mapk, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit poab anti p p38 mapk/product/Santa Cruz Biotechnology
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    Price from $9.99 to $1999.99
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    Image Search Results


    List of antibodies

    Journal: Cellular and Molecular Neurobiology

    Article Title: TMEM16A Activation Inhibits Autophagy in Dorsal Root Ganglion Cells, Which is Associated with the p38 MAPK/mTOR Pathway

    doi: 10.1007/s10571-024-01507-z

    Figure Lengend Snippet: List of antibodies

    Article Snippet: Rabbit Anti p-p38/MAPK (Thr180/Tyr182) (Proteintech) , 28796-1-AP , 1:2000.

    Techniques: Labeling

    ( A – C ) TMEM16A increases mRNA expression of p38 MAPK and mTOR (n = 10); ( D – H ) TMEM16A enhances protein expression of p38 MAPK and mTOR (n = 10). * Compared with control, P < 0.05; # Compared with NC+Rap, P < 0.05; +si-TMEM16A + Rap compared with TMEM16A+oe+Rap, P < 0.05

    Journal: Cellular and Molecular Neurobiology

    Article Title: TMEM16A Activation Inhibits Autophagy in Dorsal Root Ganglion Cells, Which is Associated with the p38 MAPK/mTOR Pathway

    doi: 10.1007/s10571-024-01507-z

    Figure Lengend Snippet: ( A – C ) TMEM16A increases mRNA expression of p38 MAPK and mTOR (n = 10); ( D – H ) TMEM16A enhances protein expression of p38 MAPK and mTOR (n = 10). * Compared with control, P < 0.05; # Compared with NC+Rap, P < 0.05; +si-TMEM16A + Rap compared with TMEM16A+oe+Rap, P < 0.05

    Article Snippet: Rabbit Anti p-p38/MAPK (Thr180/Tyr182) (Proteintech) , 28796-1-AP , 1:2000.

    Techniques: Expressing, Control

    IL-33 Inhibits the expression of tight junction proteins in BMEC and enhances activation of the p38 signaling pathway. ( A ) IL-33 suppresses the expression of Claudin-5 and can cause abnormal distribution of Claudin-5. ( B ) Relative protein expression of Claudin-5. ( C ) Immunofluorescence analysis method is used to examine the expression and distribution of Claudin-5 in hCMEC/D3 due to IL-33. The working concentration of IL-33 is 10 ng/mL. Bar, 10 µM. ( D ) IL-33 promotes the expression of MMP-9 and phosphorylation of p38 in hCMEC/D3. ( E ) Grayscale analysis of the expression of MMP-9. ( F ) Grayscale analysis of the expression of p38, and phosphorylated p38. ( G ) MMP-9 expression in cells treatment with IL-33 was measured using ELISA ( n = 3). The data are presented as the mean ± standard deviation (SD) and were analyzed by one-way ANOVA. ** P < 0.01, * P < 0.05.

    Journal: Microbiology Spectrum

    Article Title: Exploring the destructive synergy between IL-33 and Suilysin hemolysis on blood-brain barrier stability

    doi: 10.1128/spectrum.00612-24

    Figure Lengend Snippet: IL-33 Inhibits the expression of tight junction proteins in BMEC and enhances activation of the p38 signaling pathway. ( A ) IL-33 suppresses the expression of Claudin-5 and can cause abnormal distribution of Claudin-5. ( B ) Relative protein expression of Claudin-5. ( C ) Immunofluorescence analysis method is used to examine the expression and distribution of Claudin-5 in hCMEC/D3 due to IL-33. The working concentration of IL-33 is 10 ng/mL. Bar, 10 µM. ( D ) IL-33 promotes the expression of MMP-9 and phosphorylation of p38 in hCMEC/D3. ( E ) Grayscale analysis of the expression of MMP-9. ( F ) Grayscale analysis of the expression of p38, and phosphorylated p38. ( G ) MMP-9 expression in cells treatment with IL-33 was measured using ELISA ( n = 3). The data are presented as the mean ± standard deviation (SD) and were analyzed by one-way ANOVA. ** P < 0.01, * P < 0.05.

    Article Snippet: Primary antibodies used included rabbit anti-Claudin-5 (Thermo Fisher, 35-2500), rabbit anti-p38 MAPK (Cell Signaling Technology, 8690), and rabbit anti-p-p38 MAPK (Cell Signaling Technology, 4511), each at a dilution of 1:3,000.

    Techniques: Expressing, Activation Assay, Immunofluorescence, Concentration Assay, Enzyme-linked Immunosorbent Assay, Standard Deviation

    The IL-33/ST2 axis mediates the disruption of the BBB model by Sly hemolytic products. ( A ) TEER method to detect the role of IL-33/ST2 signaling in the process of BBB disruption by Sly hemolytic products. ( B ) MMP-9 mediates the suppression of Claudin-5 expression by IL-33. AMPM, p38 inhibitor Adezmapimod (SB203580). MMST, MMP-9 inhibitor, Marimastat (BB-2516). ( C ) Relative protein expression of Claudin-5. ( D and E ) The p38 signaling pathway mediates the promotion of IL-6 and IL-8 expression by IL-33. The data are presented as the mean ± standard deviation (SD) and were analyzed by one-way ANOVA. ** P < 0.01, * P < 0.05.

    Journal: Microbiology Spectrum

    Article Title: Exploring the destructive synergy between IL-33 and Suilysin hemolysis on blood-brain barrier stability

    doi: 10.1128/spectrum.00612-24

    Figure Lengend Snippet: The IL-33/ST2 axis mediates the disruption of the BBB model by Sly hemolytic products. ( A ) TEER method to detect the role of IL-33/ST2 signaling in the process of BBB disruption by Sly hemolytic products. ( B ) MMP-9 mediates the suppression of Claudin-5 expression by IL-33. AMPM, p38 inhibitor Adezmapimod (SB203580). MMST, MMP-9 inhibitor, Marimastat (BB-2516). ( C ) Relative protein expression of Claudin-5. ( D and E ) The p38 signaling pathway mediates the promotion of IL-6 and IL-8 expression by IL-33. The data are presented as the mean ± standard deviation (SD) and were analyzed by one-way ANOVA. ** P < 0.01, * P < 0.05.

    Article Snippet: Primary antibodies used included rabbit anti-Claudin-5 (Thermo Fisher, 35-2500), rabbit anti-p38 MAPK (Cell Signaling Technology, 8690), and rabbit anti-p-p38 MAPK (Cell Signaling Technology, 4511), each at a dilution of 1:3,000.

    Techniques: Disruption, Expressing, Standard Deviation

    Evidence that p38 is critical for CPC-induced paraptosis (A) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC for 24 h. (B and C) Cytotoxicity of MIAPaCa2 and SW1990 cells treated with CPC in the absence or presence of the GS4997 (10 μM) or doramapimod (5 μM) for 24 h. (D) MIAPaCa2 and SW1990 cells were treated with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h. ER structures were stained with ER-Tracker Red. Scale bar: 10 μm. (E) Light microscopy analysis of cell morphology in indicated MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h, followed by quantitative assessment. (F–H) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of tauroursodeoxycholate (TUDC; 1 mM), 4μ8C (100 μM), or GS4997 (10 μM) for 24 h. Data are presented as mean ± SD. The proportion of cells displaying vacuoles was determined by visually examining a minimum of 100 cells, and the data are presented as the mean ± SD from at least three independent experiments (E). p values were calculated by one-way ANOVA (A, E, F, G, and H) or two-way ANOVA (B and C). See also <xref ref-type=Figure S4 . " width="100%" height="100%">

    Journal: iScience

    Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway

    doi: 10.1016/j.isci.2024.110598

    Figure Lengend Snippet: Evidence that p38 is critical for CPC-induced paraptosis (A) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC for 24 h. (B and C) Cytotoxicity of MIAPaCa2 and SW1990 cells treated with CPC in the absence or presence of the GS4997 (10 μM) or doramapimod (5 μM) for 24 h. (D) MIAPaCa2 and SW1990 cells were treated with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h. ER structures were stained with ER-Tracker Red. Scale bar: 10 μm. (E) Light microscopy analysis of cell morphology in indicated MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of GS4997 (10 μM) or doramapimod (5 μM) for 24 h, followed by quantitative assessment. (F–H) Western blot analysis of protein expression in MIAPaCa2 and SW1990 cells after treatment with CPC (7.5 μM) in the absence or presence of tauroursodeoxycholate (TUDC; 1 mM), 4μ8C (100 μM), or GS4997 (10 μM) for 24 h. Data are presented as mean ± SD. The proportion of cells displaying vacuoles was determined by visually examining a minimum of 100 cells, and the data are presented as the mean ± SD from at least three independent experiments (E). p values were calculated by one-way ANOVA (A, E, F, G, and H) or two-way ANOVA (B and C). See also Figure S4 .

    Article Snippet: Rabbit polyclonal anti-p-p38 MAPK (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID: AB_2918205.

    Techniques: Western Blot, Expressing, Staining, Light Microscopy

    CPC suppresses pancreatic cancer tumor growth in vivo (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of human PANC1 cells (CDXs) or PDXs in immunocompromised NSG-SCID mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). CDX models involve the transplantation of established cancer cell lines into mice. PDX models involve the transplantation of cancerous tissue or isolated cells from a patient into immunocompromised mice. (B and C) Tumor growth curves of CDXs or PDXs implanted subcutaneously into NSG-SCID mice ( n = 5 mice per group). (D) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). An orthotopic model of pancreatic cancer is a specific type of animal model where pancreatic cancer cells or tissues are surgically implanted into the pancreas of the host animal. (E) Survival curves of indicated mice treated with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod ( n = 10 mice/group). (F) A schematic diagram illustrating the experimental setup involving the KPC mice followed by a 6-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). (G) Survival curves of indicated mice treated with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod ( n = 10 mice/group). (H–J) Pancreatic sections from KPC mice, following 4 weeks of treatment with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod, were subjected to trichrome staining to visualize both the structural changes and stromal response. Quantification of relative expression was performed ( n = 5 mice/group) using one-way ANOVA with Tukey’s multiple comparisons test. The results are presented as mean ± SD. (K) A schematic diagram illustrating how CPC-induced paraptosis contributes to the eradication of pancreatic cancer via the ERN1-MAP3K5-p38 pathway.

    Journal: iScience

    Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway

    doi: 10.1016/j.isci.2024.110598

    Figure Lengend Snippet: CPC suppresses pancreatic cancer tumor growth in vivo (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of human PANC1 cells (CDXs) or PDXs in immunocompromised NSG-SCID mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). CDX models involve the transplantation of established cancer cell lines into mice. PDX models involve the transplantation of cancerous tissue or isolated cells from a patient into immunocompromised mice. (B and C) Tumor growth curves of CDXs or PDXs implanted subcutaneously into NSG-SCID mice ( n = 5 mice per group). (D) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). An orthotopic model of pancreatic cancer is a specific type of animal model where pancreatic cancer cells or tissues are surgically implanted into the pancreas of the host animal. (E) Survival curves of indicated mice treated with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod ( n = 10 mice/group). (F) A schematic diagram illustrating the experimental setup involving the KPC mice followed by a 6-week treatment protocol. During this period, the mice received either a vehicle or CPC (10 mg/kg orally, once daily, 5 days per week), under conditions with or without 4μ8C (20 mg/kg orally, once daily, 5 days per week), GS4997 (10 mg/kg orally, once daily, 5 days per week), or doramapimod (20 mg/kg orally, once daily, 5 days per week). (G) Survival curves of indicated mice treated with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod ( n = 10 mice/group). (H–J) Pancreatic sections from KPC mice, following 4 weeks of treatment with vehicle, CPC, 4μ8C, GS4997, and/or doramapimod, were subjected to trichrome staining to visualize both the structural changes and stromal response. Quantification of relative expression was performed ( n = 5 mice/group) using one-way ANOVA with Tukey’s multiple comparisons test. The results are presented as mean ± SD. (K) A schematic diagram illustrating how CPC-induced paraptosis contributes to the eradication of pancreatic cancer via the ERN1-MAP3K5-p38 pathway.

    Article Snippet: Rabbit polyclonal anti-p-p38 MAPK (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID: AB_2918205.

    Techniques: In Vivo, Transplantation Assay, Isolation, Animal Model, Staining, Expressing

    Journal: iScience

    Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway

    doi: 10.1016/j.isci.2024.110598

    Figure Lengend Snippet:

    Article Snippet: Rabbit polyclonal anti-p-p38 MAPK (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID: AB_2918205.

    Techniques: Recombinant, Lysis, Modification, Polyacrylamide Gel Electrophoresis, Protease Inhibitor, CCK-8 Assay, Sequencing, Software