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p38 α mapk  (MedChemExpress)


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    MedChemExpress p38 α mapk
    P38 α Mapk, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p38+%CE%B1+mapk/p38-%CE%B1+MAPK-IN-1/pm41429604-202-35-37
    Average 93 stars, based on 2 article reviews
    p38 α mapk - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Phospho-proteomics:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Activity Assay:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Derivative Assay:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Titration:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Western Blot:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Activation Assay:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Inhibition:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.

    Expressing:

    Article Title: Small Gold Nanoparticles Alleviate Huntington's Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1.
    Article Snippet: Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).Part 2: Roles of p38α and Pyruvate Dehydrogenase Kinase 1 (PDK1).. To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/ kg. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.. At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.At the age of Week 11, mice took the open field test and rotarod test again before sacrifice.

    Article Title: Small Gold Nanoparticles Alleviate Huntington’s Disease via Modulating p38α Mitogen-Activated Protein Kinase and Pyruvate Dehydrogenase Kinase 1
    Article Snippet: To test the therapeutic role of selected kinases, R6/2 mice received daily i.p. injections of either (i) 0.1 mL of a vehicle (10% DMSO, 25% PEG 400 and 5% dextrose) containing an inhibitor of p38α called “p38-α MAPK-IN-1” (MedChemExpress) at a dose of 2.6 mg/kg, or (ii) 0.1 mL of D5W containing an inhibitor of PDK1, sodium dichloroacetate (DCA; Sigma, 347795) at a dose of 100 mg/kg.. At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.At Weeks 6, 7, and 9, R6/2 mice underwent the open field test and rotarod test as described above.



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    Image Search Results


    ( a-d ) Migration analysis of MCF7 cells expressing NISCH WT or C185S. ( a ) Analysis of NISCH knockout (KO) in MCF7 cells (left, n = 3), and cell migration analysis (right, n = 3) after CRISPR/Cas9-based NISCH KO. ( b ) The wound-healing migration analysis. MCF7-NISCH KO (MCF7 NIS−KO ) cells re-expressing NISCH WT or C185S (MCF7-NISCH WT or C185S) were incubated in high glucose (HG, 25 mM) or low glucose (LG, 5 mM) (n = 6). The yellow color indicates the area without cells. ( c ) Single-cell migration analysis. MCF7-NISCH WT or C185S cells in LG or HG were monitored by confocal microscopy every 10 min (0–180 min). The images were combined to analyze the migration of individual cells (n = 8–10). ( d ) Transwell migration analysis. MCF7-NISCH WT or C185S cells were incubated in LG or HG for 24 h (n = 3). ( e ) Spheroid invasion analysis of MCF7-NISCH WT or C185S. Individual spheroids were incubated in HG or LG and monitored daily for 96 h (n = 10). Data represent the mean ± SD. The statistical difference was analyzed by one-way ANOVA and Tukey’s post-hoc test ( a , c ) or two-way ANOVA and Sidak’s post-hoc test ( b , d-e ), where *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Journal: Free radical biology & medicine

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation

    doi: 10.1016/j.freeradbiomed.2025.11.013

    Figure Lengend Snippet: ( a-d ) Migration analysis of MCF7 cells expressing NISCH WT or C185S. ( a ) Analysis of NISCH knockout (KO) in MCF7 cells (left, n = 3), and cell migration analysis (right, n = 3) after CRISPR/Cas9-based NISCH KO. ( b ) The wound-healing migration analysis. MCF7-NISCH KO (MCF7 NIS−KO ) cells re-expressing NISCH WT or C185S (MCF7-NISCH WT or C185S) were incubated in high glucose (HG, 25 mM) or low glucose (LG, 5 mM) (n = 6). The yellow color indicates the area without cells. ( c ) Single-cell migration analysis. MCF7-NISCH WT or C185S cells in LG or HG were monitored by confocal microscopy every 10 min (0–180 min). The images were combined to analyze the migration of individual cells (n = 8–10). ( d ) Transwell migration analysis. MCF7-NISCH WT or C185S cells were incubated in LG or HG for 24 h (n = 3). ( e ) Spheroid invasion analysis of MCF7-NISCH WT or C185S. Individual spheroids were incubated in HG or LG and monitored daily for 96 h (n = 10). Data represent the mean ± SD. The statistical difference was analyzed by one-way ANOVA and Tukey’s post-hoc test ( a , c ) or two-way ANOVA and Sidak’s post-hoc test ( b , d-e ), where *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Article Snippet: The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C.

    Techniques: Migration, Expressing, Knock-Out, CRISPR, Incubation, Confocal Microscopy

    ( a ) A scheme of the G-PROV approach that enables functional analysis of glutathionylation on the protein of interest (POI): dehydroglutathione (dhG) is used to introduce a non-reducible glutathione modification on the purified engineered NISCH construct (enNISCH). Subsequently, the glutathione-modified NISCH construct is delivered to cells via fusogenic liposome, where the effect of glutathionylation on NISCH can be analyzed. ( b ) dhG modification on purified enNISCH. Purified enNISCH WT and C185S were incubated with dhG. The dhG-mediated glutathione modification was analyzed by glutathione antibody (n = 2). ( c ) Analysis of enNISCH delivered to MDA-MB-231 cells via fusogenic liposome. After incubating fusogenic liposomes containing His-enNISCH constructs (modified or non-modified by dhG) for 2 h, lysates were analyzed by Western blot (n = 2). ( d-e ) The migration and invasion assays. After incubating fusogenic liposomes for 2 h, MDA-MB-231 cells were analyzed by the wound-healing migration ( d , n = 6) and transwell invasion ( e , n = 2) assays. ( f ) The colony formation by enNISCH constructs. Fusogenic liposomes containing enNISCH WT or C185S were incubated with MDA-MB-231 cells on plates, and the number of colonies formed was counted after 15 days. Cells were incubated in DMEM containing 25 mM Glc ( d – e ) or 5 mM Glc ( f ). The statistical difference was analyzed by one-way ANOVA and Tukey’s post-hoc test ( b – e ) or two-way ANOVA and Sidak’s post-hoc test ( f ), where *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Journal: Free radical biology & medicine

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation

    doi: 10.1016/j.freeradbiomed.2025.11.013

    Figure Lengend Snippet: ( a ) A scheme of the G-PROV approach that enables functional analysis of glutathionylation on the protein of interest (POI): dehydroglutathione (dhG) is used to introduce a non-reducible glutathione modification on the purified engineered NISCH construct (enNISCH). Subsequently, the glutathione-modified NISCH construct is delivered to cells via fusogenic liposome, where the effect of glutathionylation on NISCH can be analyzed. ( b ) dhG modification on purified enNISCH. Purified enNISCH WT and C185S were incubated with dhG. The dhG-mediated glutathione modification was analyzed by glutathione antibody (n = 2). ( c ) Analysis of enNISCH delivered to MDA-MB-231 cells via fusogenic liposome. After incubating fusogenic liposomes containing His-enNISCH constructs (modified or non-modified by dhG) for 2 h, lysates were analyzed by Western blot (n = 2). ( d-e ) The migration and invasion assays. After incubating fusogenic liposomes for 2 h, MDA-MB-231 cells were analyzed by the wound-healing migration ( d , n = 6) and transwell invasion ( e , n = 2) assays. ( f ) The colony formation by enNISCH constructs. Fusogenic liposomes containing enNISCH WT or C185S were incubated with MDA-MB-231 cells on plates, and the number of colonies formed was counted after 15 days. Cells were incubated in DMEM containing 25 mM Glc ( d – e ) or 5 mM Glc ( f ). The statistical difference was analyzed by one-way ANOVA and Tukey’s post-hoc test ( b – e ) or two-way ANOVA and Sidak’s post-hoc test ( f ), where *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Article Snippet: The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C.

    Techniques: Functional Assay, Introduce, Modification, Purification, Construct, Incubation, Liposomes, Western Blot, Migration

    PTPRK activated the DUSP1/p38 MAPK signaling pathway in PHN. A , Western blot was performed to analyze the protein levels of DUSP1, p-p38 MAPK, and p38 MAPK in DRG tissues of each group; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in Lv-NC and Lv-PTPRK groups were detected via Western blot. ( N = 5).

    Journal: Scientific Reports

    Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia

    doi: 10.1038/s41598-025-24233-y

    Figure Lengend Snippet: PTPRK activated the DUSP1/p38 MAPK signaling pathway in PHN. A , Western blot was performed to analyze the protein levels of DUSP1, p-p38 MAPK, and p38 MAPK in DRG tissues of each group; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in Lv-NC and Lv-PTPRK groups were detected via Western blot. ( N = 5).

    Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

    Techniques: Western Blot

    p38 MAPK signaling pathway activation promoted mechanical allodynia and inflammation in rat DRG tissues. A , Paw withdrawal thresholds and B , paw withdrawal latency in each group were quantified; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG tissues of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG tissues of each group. ( N = 5; ** p < 0.01 vs. the RTX-PHN + Lv-shNC group; # p < 0.05, ## p < 0.01 vs. the RTX-PHN + Lv-shPTPRK group).

    Journal: Scientific Reports

    Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia

    doi: 10.1038/s41598-025-24233-y

    Figure Lengend Snippet: p38 MAPK signaling pathway activation promoted mechanical allodynia and inflammation in rat DRG tissues. A , Paw withdrawal thresholds and B , paw withdrawal latency in each group were quantified; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG tissues of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG tissues of each group. ( N = 5; ** p < 0.01 vs. the RTX-PHN + Lv-shNC group; # p < 0.05, ## p < 0.01 vs. the RTX-PHN + Lv-shPTPRK group).

    Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

    Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    PTPRK overexpression promoted inflammation via activating DUSP1/p38 MAPK signaling pathway in rat DRG cells. A , PTPRK expression was analyzed by RT-qPCR after empty and PTPRK overexpression vectors transfection; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in each group were detected though Western blot; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG cells of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG cells of each group. ( N = 3; ** p < 0.01 vs. the vector group; ## p < 0.01 vs. the PTPRK group).

    Journal: Scientific Reports

    Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia

    doi: 10.1038/s41598-025-24233-y

    Figure Lengend Snippet: PTPRK overexpression promoted inflammation via activating DUSP1/p38 MAPK signaling pathway in rat DRG cells. A , PTPRK expression was analyzed by RT-qPCR after empty and PTPRK overexpression vectors transfection; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in each group were detected though Western blot; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG cells of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG cells of each group. ( N = 3; ** p < 0.01 vs. the vector group; ## p < 0.01 vs. the PTPRK group).

    Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

    Techniques: Over Expression, Expressing, Quantitative RT-PCR, Transfection, Western Blot, Enzyme-linked Immunosorbent Assay, Plasmid Preparation

    Effects of vancomycin (Vanco) and lycopene (Lyco) administrations on (A) nuclear factor kappa B (NF‐κB), (B) tumour necrosis factor‐alpha (TNF‐ α ), (C) B‐cell lymphoma 3 (Bcl‐3) and (D) mitogen‐activated protein kinase p38 alpha (p38 α MAPK) levels in kidney tissues of rats. Values are given as mean ± SD CO Control versus others: * p < 0.05, ** p < 0.01, *** p < 0.001; Vanco versus others: # p < 0.05, ## p < 0.01, ### p < 0.001; Vanco + Lyco 5 versus Vanco + Lyco 10: & p < 0.05, && p < 0.01, &&& p < 0.001.

    Journal: Basic & Clinical Pharmacology & Toxicology

    Article Title: Antioxidant, Antiinflammatory and Antiapoptotic Effects of Lycopene in Rats With Vancomycin‐Induced Nephrotoxicity

    doi: 10.1111/bcpt.70084

    Figure Lengend Snippet: Effects of vancomycin (Vanco) and lycopene (Lyco) administrations on (A) nuclear factor kappa B (NF‐κB), (B) tumour necrosis factor‐alpha (TNF‐ α ), (C) B‐cell lymphoma 3 (Bcl‐3) and (D) mitogen‐activated protein kinase p38 alpha (p38 α MAPK) levels in kidney tissues of rats. Values are given as mean ± SD CO Control versus others: * p < 0.05, ** p < 0.01, *** p < 0.001; Vanco versus others: # p < 0.05, ## p < 0.01, ### p < 0.001; Vanco + Lyco 5 versus Vanco + Lyco 10: & p < 0.05, && p < 0.01, &&& p < 0.001.

    Article Snippet: Nuclear Factor kappa B (NF‐κB; product no: SEB824Ra), tumour necrosis factor‐alpha (TNF‐ α ; product no: SEA133Ra) and B‐cell lymphoma 3 (Bcl‐3; Product No: SEB734Ra) levels (Cloud‐Clone Corp. [CCC, TX, USA]) and mitogen‐activated protein kinase p38 alpha ([p38 α MAPK; Catalogue No: CK‐bio‐25 173], Shanghai Coon Koon Biotech Co Ltd. [Shanghai, China]) activity were decided with commercial ELISA kits consistent with the manufacturer's instructions.

    Techniques: Control

    RBP7 KD-induced cell proliferation inhibition depends on p38 MAPK pathway activation. (A) Western blot analysis showing the effects of RBP7 KD on p38 MAPK pathway in HCC cells. (B) Western blot result showing the effect of p38 siRNA transfection on RBP7 KD-induced changes in apoptosis-related proteins in Huh7 cells. (C) Cell count to analyze the effect of p38 siRNA transfection on RBP7 KD-induced cell proliferation inhibition in Huh7 cells. All experiments were performed at least three times. Data are shown as mean ± standard deviations. P values were calculated using Student’s t test; ** P < 0.01 and *** P < 0.001 compare to siNC; ### P < 0.001.

    Journal: Frontiers in Oncology

    Article Title: RBP7 knockdown inhibits proliferation of human hepatocellular carcinoma and activates the p38 MAPK pathway

    doi: 10.3389/fonc.2025.1592616

    Figure Lengend Snippet: RBP7 KD-induced cell proliferation inhibition depends on p38 MAPK pathway activation. (A) Western blot analysis showing the effects of RBP7 KD on p38 MAPK pathway in HCC cells. (B) Western blot result showing the effect of p38 siRNA transfection on RBP7 KD-induced changes in apoptosis-related proteins in Huh7 cells. (C) Cell count to analyze the effect of p38 siRNA transfection on RBP7 KD-induced cell proliferation inhibition in Huh7 cells. All experiments were performed at least three times. Data are shown as mean ± standard deviations. P values were calculated using Student’s t test; ** P < 0.01 and *** P < 0.001 compare to siNC; ### P < 0.001.

    Article Snippet: The antibodies were shown as follows: rabbit α-RBP7 (A15939, ABclonal, Woburn, USA), mouse α-cyclin D1 (60186-1-lg, Proteintech, Rosemont, USA), rabbit α-cyclin A2 (18202-1-AP, Proteintech), rabbit α-PARP1 (66520-1-lg, Proteintech), rabbit α-caspase 9 (#9661, CST), rabbit α-cleaved caspase 7 (#9661, CST), rabbit α-cleaved caspase 3 (#9661, CST), rabbit α-p38 (#8690, CST), rabbit α-p-p38 (#4511, CST, Boston, USA) and secondary antibodies (S0001 and S0002, Affinity Biosciences, Changzhou, China).

    Techniques: Inhibition, Activation Assay, Western Blot, Transfection, Cell Counting

    RBP7 KD-induced cell proliferation inhibition depends on p38 MAPK pathway activation. (A) Western blot analysis showing the effects of RBP7 KD on p38 MAPK pathway in HCC cells. (B) Western blot result showing the effect of p38 siRNA transfection on RBP7 KD-induced changes in apoptosis-related proteins in Huh7 cells. (C) Cell count to analyze the effect of p38 siRNA transfection on RBP7 KD-induced cell proliferation inhibition in Huh7 cells. All experiments were performed at least three times. Data are shown as mean ± standard deviations. P values were calculated using Student’s t test; ** P < 0.01 and *** P < 0.001 compare to siNC; ### P < 0.001.

    Journal: Frontiers in Oncology

    Article Title: RBP7 knockdown inhibits proliferation of human hepatocellular carcinoma and activates the p38 MAPK pathway

    doi: 10.3389/fonc.2025.1592616

    Figure Lengend Snippet: RBP7 KD-induced cell proliferation inhibition depends on p38 MAPK pathway activation. (A) Western blot analysis showing the effects of RBP7 KD on p38 MAPK pathway in HCC cells. (B) Western blot result showing the effect of p38 siRNA transfection on RBP7 KD-induced changes in apoptosis-related proteins in Huh7 cells. (C) Cell count to analyze the effect of p38 siRNA transfection on RBP7 KD-induced cell proliferation inhibition in Huh7 cells. All experiments were performed at least three times. Data are shown as mean ± standard deviations. P values were calculated using Student’s t test; ** P < 0.01 and *** P < 0.001 compare to siNC; ### P < 0.001.

    Article Snippet: The antibodies were shown as follows: rabbit α-RBP7 (A15939, ABclonal, Woburn, USA), mouse α-cyclin D1 (60186-1-lg, Proteintech, Rosemont, USA), rabbit α-cyclin A2 (18202-1-AP, Proteintech), rabbit α-PARP1 (66520-1-lg, Proteintech), rabbit α-caspase 9 (#9661, CST), rabbit α-cleaved caspase 7 (#9661, CST), rabbit α-cleaved caspase 3 (#9661, CST), rabbit α-p38 (#8690, CST), rabbit α-p-p38 (#4511, CST, Boston, USA) and secondary antibodies (S0001 and S0002, Affinity Biosciences, Changzhou, China).

    Techniques: Inhibition, Activation Assay, Western Blot, Transfection, Cell Counting