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Bioss p p38mapk
Effects of OST on cardiac autophagy and the <t>p38MAPK/mTOR</t> signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.
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Cell Signaling Technology Inc p p38
Effects of OST on cardiac autophagy and the <t>p38MAPK/mTOR</t> signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.
P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Abmart Inc p p38 mapk rabbit ab
The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, <t>p38,</t> PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.
P P38 Mapk Rabbit Ab, supplied by Abmart 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 p p38 4511s antibodies
YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and <t>p38</t> signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.
P P38 4511s Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+p38+mapk/Phospho-p38+MAPK+(Thr180%2FTyr182)+XP+Rabbit+mAb/pmc12914111-38-10-16
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Proteintech p p38 mapk polyclonal antibody
Itaconate Regulates Lysosomal Function, Calcium Signaling, and <t>p38</t> MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification <t>of</t> <t>p-p38</t> and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.
P P38 Mapk Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc p p38 mapk
MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of <t>p-p38</t> and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.
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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Proteintech p p38
tRNA synthetase inhibition causes persistent ribosome stalls. ( A ) U-2 OS cells expressing GFP-G3BP1 were treated with 20 µM halofuginone (HF) or 0.2% DMSO carrier. Images were collected every 2 h for 16 h and representative images are shown ( n = 3 independent experiments). ( B ) Cells were treated with DMSO (−) or 20 µM HF for 4 or 16 h, and P-eIF2α and total eIF2α were detected by Western blotting. Representative blots with total protein are shown at the left , and the average ± SEM of n = 3 independent experiments is shown at the right . Molecular weights (in kilodaltons) are shown. ( C ) Cells were treated with 20 µM HF for 1 h (black line), 4 h (purple line), or 16 h (green line), and polysome profiling was performed. A representative profile is shown at the left , and the average ± SEM of the polysome:monosome ratio from n = 3 independent replicates is shown at the right . Pink, gray, and green dots represent results from each replicate. ( D ) Cells were treated with either 0.2% DMSO carrier or 20 µM HF in the presence or absence of 250 µM sodium arsenite (As) or 2 µM rocaglamide A (RocA), and GFP-G3BP1 was imaged every 0.5 h for 3 h. Representative images are shown at the left with the average ± SEM. The percentage of cells with SGs from n = 3 independent experiments is shown at the right ; ≥288 cells were counted per treatment across all replicates. ( E ) Cells were treated with 0.2% DMSO (black line), 2 µM RocA (green line), or 2 µM RocA plus 20 µM HF (purple line) for 3 h followed by polysome profiling. Representative profiles are shown at the left , and the average ± SEM from n = 3 independent experiments is shown at the right , with pink, gray, and green dots representing each replicate. ( F ) Cells were untreated (DMSO carrier) or treated for 24, 4, or 1 h with 20 µM anisomycin (ANI) or 20 µM halofuginone, and Western blotting for <t>p-p38</t> and p-JNK was done, with the total protein shown below . A representative blot of n = 2 independent experiments is shown. Scale bars, 10 µm. Significance was assessed with ordinary one-way ANOVAs and Tukey's multiple comparisons tests. (*) P < 0.05, (**) P < 0.01, (***) P < 0.005.
P P38, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+p38+mapk/p38+MAPK+Antibody/pmc13041551-12-0-3
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Proteintech anti p p38 mapk
tRNA synthetase inhibition causes persistent ribosome stalls. ( A ) U-2 OS cells expressing GFP-G3BP1 were treated with 20 µM halofuginone (HF) or 0.2% DMSO carrier. Images were collected every 2 h for 16 h and representative images are shown ( n = 3 independent experiments). ( B ) Cells were treated with DMSO (−) or 20 µM HF for 4 or 16 h, and P-eIF2α and total eIF2α were detected by Western blotting. Representative blots with total protein are shown at the left , and the average ± SEM of n = 3 independent experiments is shown at the right . Molecular weights (in kilodaltons) are shown. ( C ) Cells were treated with 20 µM HF for 1 h (black line), 4 h (purple line), or 16 h (green line), and polysome profiling was performed. A representative profile is shown at the left , and the average ± SEM of the polysome:monosome ratio from n = 3 independent replicates is shown at the right . Pink, gray, and green dots represent results from each replicate. ( D ) Cells were treated with either 0.2% DMSO carrier or 20 µM HF in the presence or absence of 250 µM sodium arsenite (As) or 2 µM rocaglamide A (RocA), and GFP-G3BP1 was imaged every 0.5 h for 3 h. Representative images are shown at the left with the average ± SEM. The percentage of cells with SGs from n = 3 independent experiments is shown at the right ; ≥288 cells were counted per treatment across all replicates. ( E ) Cells were treated with 0.2% DMSO (black line), 2 µM RocA (green line), or 2 µM RocA plus 20 µM HF (purple line) for 3 h followed by polysome profiling. Representative profiles are shown at the left , and the average ± SEM from n = 3 independent experiments is shown at the right , with pink, gray, and green dots representing each replicate. ( F ) Cells were untreated (DMSO carrier) or treated for 24, 4, or 1 h with 20 µM anisomycin (ANI) or 20 µM halofuginone, and Western blotting for <t>p-p38</t> and p-JNK was done, with the total protein shown below . A representative blot of n = 2 independent experiments is shown. Scale bars, 10 µm. Significance was assessed with ordinary one-way ANOVAs and Tukey's multiple comparisons tests. (*) P < 0.05, (**) P < 0.01, (***) P < 0.005.
Anti P P38 Mapk, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Effects of OST on cardiac autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Effects of OST on cardiac autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques: Transmission Assay, Electron Microscopy, Western Blot

Effects of OST on autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice after SB203580 administration. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-mTOR and mTOR. (H) Quantitative analysis of p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). # P < 0.05, ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group; ▲ P < 0.05, ▲▲ P < 0.01 vs the TRZ + OST H group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Effects of OST on autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice after SB203580 administration. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-mTOR and mTOR. (H) Quantitative analysis of p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). # P < 0.05, ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group; ▲ P < 0.05, ▲▲ P < 0.01 vs the TRZ + OST H group.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques: Transmission Assay, Electron Microscopy, Western Blot

Schematic illustration summarizing the protective effects of OST against TRZ-induced cardiotoxicity by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

doi: 10.1016/j.jtcme.2025.06.001

Figure Lengend Snippet: Schematic illustration summarizing the protective effects of OST against TRZ-induced cardiotoxicity by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.

Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

Techniques:

The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Article Snippet: p-p38 MAPK Rabbit Ab , Abmart , TA4001 , 1: 1500.

Techniques: Expressing

The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Article Snippet: p-p38 MAPK Rabbit Ab , Abmart , TA4001 , 1: 1500.

Techniques: Activity Assay

YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Article Snippet: Cyclin B (#4138), Vimentin (#5741), N-cadherin (#13116), p38 (#9212), and p-p38 (#4511S) antibodies were purchased from Cell Signaling Technology (USA).

Techniques: Protein-Protein interactions, Gene Expression, Control, Western Blot, Migration, Staining, Membrane, Standard Deviation

YHD inhibits the growth of OS in vivo . (A) The effect of YHD on tumorigenesis in nude mice. (B) The effect of YHD on tumor volume. (C) The effect of YHD on mouse weight. (D) Hematoxylin-eosin staining of the mouse tumor tissue. (E) Hematoxylin-eosin staining of the mouse lung tissue. (F) PCNA, Bcl-2, Vimentin, p-AKT, and p-P38 of the mouse tumor tissue were detected by immunohistochemistry. (G) Hematoxylin-eosin staining of the mouse heart and liver tissue. Data were presented as mean ± standard deviation ( n = 6).

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD inhibits the growth of OS in vivo . (A) The effect of YHD on tumorigenesis in nude mice. (B) The effect of YHD on tumor volume. (C) The effect of YHD on mouse weight. (D) Hematoxylin-eosin staining of the mouse tumor tissue. (E) Hematoxylin-eosin staining of the mouse lung tissue. (F) PCNA, Bcl-2, Vimentin, p-AKT, and p-P38 of the mouse tumor tissue were detected by immunohistochemistry. (G) Hematoxylin-eosin staining of the mouse heart and liver tissue. Data were presented as mean ± standard deviation ( n = 6).

Article Snippet: Cyclin B (#4138), Vimentin (#5741), N-cadherin (#13116), p38 (#9212), and p-p38 (#4511S) antibodies were purchased from Cell Signaling Technology (USA).

Techniques: In Vivo, Staining, Immunohistochemistry, Standard Deviation

Itaconate Regulates Lysosomal Function, Calcium Signaling, and p38 MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification of p-p38 and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.

Journal: Redox Biology

Article Title: Stromal cell-derived itaconate promotes endometriosis via macrophage NRF2 and lysosomal pH modulation

doi: 10.1016/j.redox.2026.104101

Figure Lengend Snippet: Itaconate Regulates Lysosomal Function, Calcium Signaling, and p38 MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification of p-p38 and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.

Article Snippet: After blocking in 5% milk in TBST, membranes were incubated overnight at 4 °C with primary antibodies: Beta Actin Monoclonal antibody(1:20000, 66009-1-Ig; Proteintech), Beta Tubulin Recombinant antibody (1:5000, 80713-1-RR; Proteintech), Anti-IRG1 antibody (1:1000; ab222411; abcam; Cambridge, UK), Nrf2 monoclonal antibody (1:2000; A21176; abclonal; Wuhan, China), iNOS Polyclonal antibody (1:500; 22226-1-AP; Proteintech), NOX2 Polyclonal antibody (1:3000; 19013-1-AP; Proteintech), p-p38 MAPK Polyclonal antibody (1:2000; 28796-1-AP; Proteintech), and p38 MAPK Polyclonal antibody (1:4000; 14064-1-AP; Proteintech).

Techniques: Derivative Assay, Fluorescence, Expressing, Cell Culture, Flow Cytometry, Western Blot, Control

MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of p-p38 and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.

Journal: Oncology Letters

Article Title: Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis

doi: 10.3892/ol.2026.15551

Figure Lengend Snippet: MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of p-p38 and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.

Article Snippet: p-p38 MAPK (Thr180/Tyr182) , 4511 , 1:1,000 , Cell Signaling Technology, Inc..

Techniques: Inhibition, Luciferase, Expressing, Activity Assay, Western Blot, Colony Assay

tRNA synthetase inhibition causes persistent ribosome stalls. ( A ) U-2 OS cells expressing GFP-G3BP1 were treated with 20 µM halofuginone (HF) or 0.2% DMSO carrier. Images were collected every 2 h for 16 h and representative images are shown ( n = 3 independent experiments). ( B ) Cells were treated with DMSO (−) or 20 µM HF for 4 or 16 h, and P-eIF2α and total eIF2α were detected by Western blotting. Representative blots with total protein are shown at the left , and the average ± SEM of n = 3 independent experiments is shown at the right . Molecular weights (in kilodaltons) are shown. ( C ) Cells were treated with 20 µM HF for 1 h (black line), 4 h (purple line), or 16 h (green line), and polysome profiling was performed. A representative profile is shown at the left , and the average ± SEM of the polysome:monosome ratio from n = 3 independent replicates is shown at the right . Pink, gray, and green dots represent results from each replicate. ( D ) Cells were treated with either 0.2% DMSO carrier or 20 µM HF in the presence or absence of 250 µM sodium arsenite (As) or 2 µM rocaglamide A (RocA), and GFP-G3BP1 was imaged every 0.5 h for 3 h. Representative images are shown at the left with the average ± SEM. The percentage of cells with SGs from n = 3 independent experiments is shown at the right ; ≥288 cells were counted per treatment across all replicates. ( E ) Cells were treated with 0.2% DMSO (black line), 2 µM RocA (green line), or 2 µM RocA plus 20 µM HF (purple line) for 3 h followed by polysome profiling. Representative profiles are shown at the left , and the average ± SEM from n = 3 independent experiments is shown at the right , with pink, gray, and green dots representing each replicate. ( F ) Cells were untreated (DMSO carrier) or treated for 24, 4, or 1 h with 20 µM anisomycin (ANI) or 20 µM halofuginone, and Western blotting for p-p38 and p-JNK was done, with the total protein shown below . A representative blot of n = 2 independent experiments is shown. Scale bars, 10 µm. Significance was assessed with ordinary one-way ANOVAs and Tukey's multiple comparisons tests. (*) P < 0.05, (**) P < 0.01, (***) P < 0.005.

Journal: Genes & Development

Article Title: tRNA synthetase activity is required for stress granule and P-body assembly

doi: 10.1101/gad.353535.125

Figure Lengend Snippet: tRNA synthetase inhibition causes persistent ribosome stalls. ( A ) U-2 OS cells expressing GFP-G3BP1 were treated with 20 µM halofuginone (HF) or 0.2% DMSO carrier. Images were collected every 2 h for 16 h and representative images are shown ( n = 3 independent experiments). ( B ) Cells were treated with DMSO (−) or 20 µM HF for 4 or 16 h, and P-eIF2α and total eIF2α were detected by Western blotting. Representative blots with total protein are shown at the left , and the average ± SEM of n = 3 independent experiments is shown at the right . Molecular weights (in kilodaltons) are shown. ( C ) Cells were treated with 20 µM HF for 1 h (black line), 4 h (purple line), or 16 h (green line), and polysome profiling was performed. A representative profile is shown at the left , and the average ± SEM of the polysome:monosome ratio from n = 3 independent replicates is shown at the right . Pink, gray, and green dots represent results from each replicate. ( D ) Cells were treated with either 0.2% DMSO carrier or 20 µM HF in the presence or absence of 250 µM sodium arsenite (As) or 2 µM rocaglamide A (RocA), and GFP-G3BP1 was imaged every 0.5 h for 3 h. Representative images are shown at the left with the average ± SEM. The percentage of cells with SGs from n = 3 independent experiments is shown at the right ; ≥288 cells were counted per treatment across all replicates. ( E ) Cells were treated with 0.2% DMSO (black line), 2 µM RocA (green line), or 2 µM RocA plus 20 µM HF (purple line) for 3 h followed by polysome profiling. Representative profiles are shown at the left , and the average ± SEM from n = 3 independent experiments is shown at the right , with pink, gray, and green dots representing each replicate. ( F ) Cells were untreated (DMSO carrier) or treated for 24, 4, or 1 h with 20 µM anisomycin (ANI) or 20 µM halofuginone, and Western blotting for p-p38 and p-JNK was done, with the total protein shown below . A representative blot of n = 2 independent experiments is shown. Scale bars, 10 µm. Significance was assessed with ordinary one-way ANOVAs and Tukey's multiple comparisons tests. (*) P < 0.05, (**) P < 0.01, (***) P < 0.005.

Article Snippet: p-p38 (Thr180/Tyr182) , Proteintech , 28796 , 1:1000 (Western).

Techniques: Inhibition, Expressing, Western Blot