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p p38  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p p38
    P P38, 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/p p38/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    p p38 - by Bioz Stars, 2025-02
    86/100 stars

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    HVO attenuated OVA/LPS-induced neutrophil-dominated airway inflammation by inhibiting NETs formation and IL-17 signaling pathway. A – D Immunohistochemical representative images a in the lung tissues and quantification analysis of the expressions of MPO B , NE C and citH3 D in A . Sizes 400 × : Scale bar = 25 µm. E – F Representative western blot bands E of p-JNK, T-JNK, <t>p-P38,</t> T-P38, p-ERK, T-ERK, and β-actin in OVA/LPS-induced mouse lung tissues, and relative phosphorylated protein levels F of JNK, P38, and ERK in E. Protein expressions of p-PI3K, p-Akt, p-JNK, and p-P38 in each group. Data was presented as mean ± SEM. **** P < 0.0001, *** P < 0.001, ** P < 0.01 versus Control group. #### P < 0.0001, ### P < 0.001, ## P < 0.01, ns P > 0.05 versus OVA/LPS group
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    HVO attenuated OVA/LPS-induced neutrophil-dominated airway inflammation by inhibiting NETs formation and IL-17 signaling pathway. A – D Immunohistochemical representative images a in the lung tissues and quantification analysis of the expressions of MPO B , NE C and citH3 D in A . Sizes 400 × : Scale bar = 25 µm. E – F Representative western blot bands E of p-JNK, T-JNK, <t>p-P38,</t> T-P38, p-ERK, T-ERK, and β-actin in OVA/LPS-induced mouse lung tissues, and relative phosphorylated protein levels F of JNK, P38, and ERK in E. Protein expressions of p-PI3K, p-Akt, p-JNK, and p-P38 in each group. Data was presented as mean ± SEM. **** P < 0.0001, *** P < 0.001, ** P < 0.01 versus Control group. #### P < 0.0001, ### P < 0.001, ## P < 0.01, ns P > 0.05 versus OVA/LPS group
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    HVO attenuated OVA/LPS-induced neutrophil-dominated airway inflammation by inhibiting NETs formation and IL-17 signaling pathway. A – D Immunohistochemical representative images a in the lung tissues and quantification analysis of the expressions of MPO B , NE C and citH3 D in A . Sizes 400 × : Scale bar = 25 µm. E – F Representative western blot bands E of p-JNK, T-JNK, <t>p-P38,</t> T-P38, p-ERK, T-ERK, and β-actin in OVA/LPS-induced mouse lung tissues, and relative phosphorylated protein levels F of JNK, P38, and ERK in E. Protein expressions of p-PI3K, p-Akt, p-JNK, and p-P38 in each group. Data was presented as mean ± SEM. **** P < 0.0001, *** P < 0.001, ** P < 0.01 versus Control group. #### P < 0.0001, ### P < 0.001, ## P < 0.01, ns P > 0.05 versus OVA/LPS group
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    Image Search Results


    The antibodies used in the study

    Journal: Neural Regeneration Research

    Article Title: Enhancing m 6 A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

    doi: 10.4103/NRR.NRR-D-23-01477

    Figure Lengend Snippet: The antibodies used in the study

    Article Snippet: P-P38 , Rabbit , WB: 1:750 , Wanleibio, Shenyang, China , WLP1576 , AB 2922420.

    Techniques:

    METTL14 activates Trib2/MAPK signaling pathway in an m 6 A-dependent manner. (A) Volcano plot of upregulated and downregulated genes in the sham and 7 dpi groups. (B) The top 15 upregulated GO terms in sensorimotor neurons 7 days after SCI. (C) Relative expression of the top 10 upregulated genes in NC- Mettl14 and sh- Mettl14 treated neurons by qPCR ( n = 3 per group). (D) Western blot of TRIB2 in NC- Mettl14 and sh- Mettl14 treated neurons. (E) Quantification of relative protein expression levels in D ( n = 3 per group). (F) Pattern diagram of meRIP-qPCR for Trib2 m 6 A modified site detection. (G) m 6 A level of Trib2 in NC- Mettl14 and sh- Mettl14 treated neurons by meRIP-qPCR ( n = 3 per group). (H) Western blots of TRIB2, p-JNK and p-P38 protein expression in the sham and SCI groups. (I) Quantification of TRIB2, p-JNK and p-P38 protein expression levels in H ( n = 3 per group). (L) Representative images of neurons (NeuN, green, AF488) and TRIB2 expression (red, AF594) in the sham and SCI groups, showing that SCI increased NeuN + TRIB2 + signaling in the cerebral cortex sections. Scale bar: 50 μm. (M) Quantification of the number of TRIB2 + NeuN + cells in L ( n = 4 per group). The data are presented as means ± SD. * P < 0.05, ** P < 0.01 (unpaired t -test (C, E, G, I–K, M)). DAPI: 4′,6-Diamidino2-phenylindole; GO: gene ontology; JNK: Jun N terminal kinase; MeRIP: Methylated RNA immunoprecipitation; m 6 A: N 6 -methyladenosine; Mettl14: methyltransferase-like protein 14; MAPK: mitogen-activated protein kinase; meRIP-qPCR: m 6 A-immunoprecipitation-qPCR; NC: negative control; ns: not significant; p-JNK: phospho-JNK; p-P38: phospho-P38; qPCR: quantitative polymerase chain reaction; SCI: spinal cord injury; Sh: short hairpin; Trib2: tribbles pseudokinase 2.

    Journal: Neural Regeneration Research

    Article Title: Enhancing m 6 A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

    doi: 10.4103/NRR.NRR-D-23-01477

    Figure Lengend Snippet: METTL14 activates Trib2/MAPK signaling pathway in an m 6 A-dependent manner. (A) Volcano plot of upregulated and downregulated genes in the sham and 7 dpi groups. (B) The top 15 upregulated GO terms in sensorimotor neurons 7 days after SCI. (C) Relative expression of the top 10 upregulated genes in NC- Mettl14 and sh- Mettl14 treated neurons by qPCR ( n = 3 per group). (D) Western blot of TRIB2 in NC- Mettl14 and sh- Mettl14 treated neurons. (E) Quantification of relative protein expression levels in D ( n = 3 per group). (F) Pattern diagram of meRIP-qPCR for Trib2 m 6 A modified site detection. (G) m 6 A level of Trib2 in NC- Mettl14 and sh- Mettl14 treated neurons by meRIP-qPCR ( n = 3 per group). (H) Western blots of TRIB2, p-JNK and p-P38 protein expression in the sham and SCI groups. (I) Quantification of TRIB2, p-JNK and p-P38 protein expression levels in H ( n = 3 per group). (L) Representative images of neurons (NeuN, green, AF488) and TRIB2 expression (red, AF594) in the sham and SCI groups, showing that SCI increased NeuN + TRIB2 + signaling in the cerebral cortex sections. Scale bar: 50 μm. (M) Quantification of the number of TRIB2 + NeuN + cells in L ( n = 4 per group). The data are presented as means ± SD. * P < 0.05, ** P < 0.01 (unpaired t -test (C, E, G, I–K, M)). DAPI: 4′,6-Diamidino2-phenylindole; GO: gene ontology; JNK: Jun N terminal kinase; MeRIP: Methylated RNA immunoprecipitation; m 6 A: N 6 -methyladenosine; Mettl14: methyltransferase-like protein 14; MAPK: mitogen-activated protein kinase; meRIP-qPCR: m 6 A-immunoprecipitation-qPCR; NC: negative control; ns: not significant; p-JNK: phospho-JNK; p-P38: phospho-P38; qPCR: quantitative polymerase chain reaction; SCI: spinal cord injury; Sh: short hairpin; Trib2: tribbles pseudokinase 2.

    Article Snippet: P-P38 , Rabbit , WB: 1:750 , Wanleibio, Shenyang, China , WLP1576 , AB 2922420.

    Techniques: Expressing, Western Blot, Modification, Methylation, RNA Immunoprecipitation, Immunoprecipitation, Negative Control, Real-time Polymerase Chain Reaction

    METTL14 promotes axon regeneration by activating the Trib2/MAPK pathway. (A) Western blots of TRIB2, p-JNK and p-P38 proteins in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons. (B–D) Quantification of TRIB2, p-JNK and p-P38 protein expression levels in A ( n = 3 per group). (E–L) Relative expression of Ntrk3 , Cntf , Igf1r , NeuroD1 , Nrg1 , Pten , Cers2 , and Ptprs in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons by qPCR ( n = 3 per group). (M) Representative images of immunofluorescence staining of TUJ1 (red, AF594) in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons, showing that overexpression of TRIB2 counteracted the impact of Mettl14 knockdown. Scale bar: 100 μm. (N) Quantification of neurite length in N ( n = 4 per group). (O) Representative immunofluorescence images of the regenerative axons (TUJ1, green, AF488) on the microfluidic cultures, showing that overexpression of TRIB2 counteracted the impact of Mettl14 knockdown. Scale bar: 200 μm. (P) Quantification of total axonal length in G ( n = 4 per group). The data are presented as means ± SD. * P < 0.05, ** P < 0.01 (one-way analysis of variance followed by Tukey’s post hoc test (B–L, N, P)). Cers2: Ceramide synthase 2; Cntf: ciliary neurotrophic factor; DAPI: 4′,6-diamidino2-phenylindole; Igf1r: insulin like growth factor 1 receptor; JNK: Jun N terminal kinase; MAPK: mitogen-activated protein kinase; Mettl14: methyltransferase-like protein 14; NC: negative control; NeuroD1: neurogenic differentiation 1; Nrg1: neuregulin 1; Ntrk3: neurotrophic receptor tyrosine kinase 3; OE: over-expression; Pten: phosphatase and tensin homolog; Ptprs: protein tyrosine phosphatase receptor type S; Sh: short hairpin; Trib2: tribbles pseudokinase 2.

    Journal: Neural Regeneration Research

    Article Title: Enhancing m 6 A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

    doi: 10.4103/NRR.NRR-D-23-01477

    Figure Lengend Snippet: METTL14 promotes axon regeneration by activating the Trib2/MAPK pathway. (A) Western blots of TRIB2, p-JNK and p-P38 proteins in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons. (B–D) Quantification of TRIB2, p-JNK and p-P38 protein expression levels in A ( n = 3 per group). (E–L) Relative expression of Ntrk3 , Cntf , Igf1r , NeuroD1 , Nrg1 , Pten , Cers2 , and Ptprs in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons by qPCR ( n = 3 per group). (M) Representative images of immunofluorescence staining of TUJ1 (red, AF594) in NC- Mettl14 , sh- Mettl14 , and sh- Mettl14 +OE- Trib2 treated neurons, showing that overexpression of TRIB2 counteracted the impact of Mettl14 knockdown. Scale bar: 100 μm. (N) Quantification of neurite length in N ( n = 4 per group). (O) Representative immunofluorescence images of the regenerative axons (TUJ1, green, AF488) on the microfluidic cultures, showing that overexpression of TRIB2 counteracted the impact of Mettl14 knockdown. Scale bar: 200 μm. (P) Quantification of total axonal length in G ( n = 4 per group). The data are presented as means ± SD. * P < 0.05, ** P < 0.01 (one-way analysis of variance followed by Tukey’s post hoc test (B–L, N, P)). Cers2: Ceramide synthase 2; Cntf: ciliary neurotrophic factor; DAPI: 4′,6-diamidino2-phenylindole; Igf1r: insulin like growth factor 1 receptor; JNK: Jun N terminal kinase; MAPK: mitogen-activated protein kinase; Mettl14: methyltransferase-like protein 14; NC: negative control; NeuroD1: neurogenic differentiation 1; Nrg1: neuregulin 1; Ntrk3: neurotrophic receptor tyrosine kinase 3; OE: over-expression; Pten: phosphatase and tensin homolog; Ptprs: protein tyrosine phosphatase receptor type S; Sh: short hairpin; Trib2: tribbles pseudokinase 2.

    Article Snippet: P-P38 , Rabbit , WB: 1:750 , Wanleibio, Shenyang, China , WLP1576 , AB 2922420.

    Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Over Expression, Knockdown, Negative Control

    HVO attenuated OVA/LPS-induced neutrophil-dominated airway inflammation by inhibiting NETs formation and IL-17 signaling pathway. A – D Immunohistochemical representative images a in the lung tissues and quantification analysis of the expressions of MPO B , NE C and citH3 D in A . Sizes 400 × : Scale bar = 25 µm. E – F Representative western blot bands E of p-JNK, T-JNK, p-P38, T-P38, p-ERK, T-ERK, and β-actin in OVA/LPS-induced mouse lung tissues, and relative phosphorylated protein levels F of JNK, P38, and ERK in E. Protein expressions of p-PI3K, p-Akt, p-JNK, and p-P38 in each group. Data was presented as mean ± SEM. **** P < 0.0001, *** P < 0.001, ** P < 0.01 versus Control group. #### P < 0.0001, ### P < 0.001, ## P < 0.01, ns P > 0.05 versus OVA/LPS group

    Journal: Chinese Medicine

    Article Title: Hyssopus cuspidatus volatile oil: a potential treatment for steroid-resistant asthma via inhibition of neutrophil extracellular traps

    doi: 10.1186/s13020-025-01069-2

    Figure Lengend Snippet: HVO attenuated OVA/LPS-induced neutrophil-dominated airway inflammation by inhibiting NETs formation and IL-17 signaling pathway. A – D Immunohistochemical representative images a in the lung tissues and quantification analysis of the expressions of MPO B , NE C and citH3 D in A . Sizes 400 × : Scale bar = 25 µm. E – F Representative western blot bands E of p-JNK, T-JNK, p-P38, T-P38, p-ERK, T-ERK, and β-actin in OVA/LPS-induced mouse lung tissues, and relative phosphorylated protein levels F of JNK, P38, and ERK in E. Protein expressions of p-PI3K, p-Akt, p-JNK, and p-P38 in each group. Data was presented as mean ± SEM. **** P < 0.0001, *** P < 0.001, ** P < 0.01 versus Control group. #### P < 0.0001, ### P < 0.001, ## P < 0.01, ns P > 0.05 versus OVA/LPS group

    Article Snippet: After blocked with 5% skim milk for 2 h, the membranes were incubated with rabbit primary antibodies at 4 °C overnight: p-JNK (Beyotime), JNK (Beyotime), p-P38 (Absin), P38 (Beyotime), p-ERK (Cell Signaling Technology) and β-actin (Abbkine), ERK (Beyotime).

    Techniques: Immunohistochemical staining, Western Blot, Control