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Cell Signaling Technology Inc anti total p38
Anti Total P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 3183 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+p38+mapk/p38+MAPK+XP+Rabbit+mAb/bio_rxiv__64898__2026__03__19__712937-185-21-23
Average 97 stars, based on 3183 article reviews

anti total p38 - by Bioz Stars, 2026-10

97/100 stars

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Article Title: ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice
Article Snippet: The glomerular glycocalyx, which is a main component of endothelial surface layer (ESL), was evaluated by staining paraffin-embedded tissue with tomato lectin (L0401, SIGMA, Kanagawa, Japan). .. SDS-PAGE was performed (20–30 μg protein/lane) with antibodies against phospho-p38/MAPK (Thr180/Tyr182) (9211S, Cell signaling, Danvers, USA), total-p38/MAPK (9211, Cell signaling, Danvers, USA), phospho-VE-cadherin (Tyr658) (44-1144G, Invitrogen, Waltham, USA), total-VE-cadherin (ab33168, abcam, Cambridge, UK) and glyceraldehyde phosphate dehydrogenase (1E6D9, proteintech, Rosemont, Illinois, USA). .. Signals were detected using Amersham ECL Western Blotting Detection Reagents (Cytiva, Marlborough, MA, USA).

Pyrolysis Gas Chromatography:

Article Title: Exogenous Beta-guanidinopropionic acid administration enhances electromyostimulation-induced mitochondrial biogenesis in rat skeletal muscle
Article Snippet: .. The following antibodies were used: PGC-1α (#516–577, Millipore, CA, USA), Total OXPHOS Rodent WB Antibody Cocktail (#ab110413, Abcam, Cambridge, UK), total-p38 MAPK (#9212, Cell Signaling Technology, Danvers, MA, USA), phospho-p38 MAPK Thr180/Tyr182 (#9211, Cell Signaling Technology, Danvers, MA, USA), total-AMPKα (#2532, Cell Signaling Technology, Danvers, MA, USA), phospho-AMPKα Thr172 (#2531, Cell Signaling Technology, Danvers, MA, USA), total-CaMKII (#4436, Cell Signaling Technology, Danvers, MA, USA), totalCaMKII (#4436, Cell Signaling Technology, Danvers, MA, USA), phospho-CaMKII Thr286 (#12716, Cell Signaling Technology, Danvers, MA, USA), Calcineurin (#2614, Cell Signaling Technology, Danvers, MA, USA), DSCR1 (#sc-377507, Santa Cruz Biotechnology, Dallas, TX, USA), LC3B (#2775, Cell Signaling Technology, Danvers, MA, USA), Fbx32 (#168372 Abcam, Cambridge, UK), MuRF1 (#sc-398608 Santa Cruz Biotechnology, Dallas, TX, USA). .. The following day, the membrane was washed by TBS-T for 5 min x three, and the secondary antibody (Anti-rabbit IgG, HRP-linked Antibody, #7074, Cell Signaling Technology, Danvers, MA, USA) (Anti-mouse IgG, HRP-linked Antibody, #7076, Cell Signaling Technology Danvers, MA, USA) was added to TBS-T and incubated at room temperature for 1 h. The membrane was rewashed in TBS-T for 5 min x three, and the bands were detected using Luminata Forte Western HRP Substrate (WBLUF0500, Millipore, CA, USA) with FUSION Chemiluminescence Imaging System (M&S Instruments, Osaka, Japan).

Western Blot:

other:

Article Title: Obesogenic diet in mice leads to inflammation and oxidative stress in the mother in association with sex-specific changes in fetal development, inflammatory markers and placental transcriptome
Article Snippet: Extracted protein (50μg in 1xSDS buffer) was heated at 90°C for 5 minutes and loaded into acrylamide gels before incubated with primary antibodies against catalase (CAT, #14097, Cell Signaling, 1:5000), 3-nitrotyrosine (3-NT, #9691 Cell signaling, 1:10000), 4-hydroxynonenal (4HNE, ab46545, Abcam, 1:1000), phosphorylated NFkB p65(phospho-p65NFkB, #3033, Cell Signaling, 1:1000), total NFkB, (NFkB p65, #8242, Cell Signaling, 1:1000) phospho-p38-Mitogen-activated protein kinase (MAPK) (phospho-p38 MAPK (Thr180/Tyr182), #4511, Cell Signaling, 1:1000), and total p38-MAPK (p38 MAPK, #8690, Cell Signaling, 1:1000).

Article Title: Multiple mechanisms activate GCN2 eIF2 kinase in response to diverse stress conditions
Article Snippet: Target proteins and their primary antibodies with vendor information and experimental dilutions that were used in the immunoblot analyses include ZAK 1:1000 (Bethyl, #A301-993A), P-GCN2 (T899) 1:1000 (Abcam, #75836), total GCN2 1:1000 (Cell Signaling, #3302), P-eIF2α (S51) 1:1000 (Abcam, #32157), total eIF2α 1:1000 (Cell Signaling, #5342), P-p38 MAPK 1:2000 (Cell Signaling, #4511S), total p38 MAPK 1:2000 (Cell Signaling, #8690S), CReP 1:1000 (Proteintech, # 14634-1-AP), Actin 1:5000 (Sigma, #A5441).

Article Title: Tumor necrosis factor receptor-1 is selectively sequestered into Schwann cell extracellular vesicles where it functions as a TNFα decoy
Article Snippet: Membranes were incubated with primary antibodies that recognize phospho-p38 MAPK (rabbit polyclonal 1:1000, Cell Signaling, 9211 s) and total p38 MAPK (1:10000, Cell Signaling, 9212 s).

Article Title: Lipidomics of triglyceride-rich lipoproteins derived from hyperlipidemic patients on inflammation.
Article Snippet: © 2023 Stichting European Society for Clinical Investigation Journal Foundation.. Published by John Wiley & Sons Ltd 1Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, Sant Joan University Hospital, Universitat Rovira i Virgili.. Institut Investigacio Sanitaria Pere Virgili (IISPV), Reus, Spain 2Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Madrid, Spain 3Biosfer Teslab SL, Department of Basic Medical Sciences, Universitat Rovira i Virgili (URV), Institut d’Investigació Sanitària Pere Virgili (IISPV), Reus, Spain

Image Search Results

Proposed mechanistic model of candesartan cilexetil (CC)-affected signaling in NPC cells. A schematic diagram illustrating the mechanism of action. This study demonstrates that CC reduces Angiotensin II Type 1 Receptor (AT1R) expression and modulates downstream signaling pathways, including AKT and p38 MAPK. CC inhibits NPC cell growth and migration by interfering with cell cycle progression and the epithelial-mesenchymal transition (EMT) process.

Journal: EXCLI Journal

Article Title: Candesartan cilexetil as a repurposed therapeutic candidate for nasopharyngeal carcinoma: Integrated in vitro and in silico analyses

doi: 10.17179/excli2025-9094

Figure Lengend Snippet: Proposed mechanistic model of candesartan cilexetil (CC)-affected signaling in NPC cells. A schematic diagram illustrating the mechanism of action. This study demonstrates that CC reduces Angiotensin II Type 1 Receptor (AT1R) expression and modulates downstream signaling pathways, including AKT and p38 MAPK. CC inhibits NPC cell growth and migration by interfering with cell cycle progression and the epithelial-mesenchymal transition (EMT) process.

Article Snippet: Antibodies against AT1R, E-cadherin, N-cadherin, vimentin, Slug, total/phospho-p38 MAPK, and total/phospho-AKT were sources from Cell Signaling Technology, with β-actin as a loading control.

Techniques: Expressing, Protein-Protein interactions, Migration

AKT and p38 signaling mediate Yoda1-induced regulation of osteo/cementogenic-related molecules in cementocytes. Cells were pretreated with selective inhibitors of ERK1/2 (PD98059), JNK (JNK inhibitor II), p38 (SB203580), or AKT (AKT inhibitor IV), followed by stimulation with 5 μM Yoda1 for 6 h in the presence of each inhibitor. Expression of Wnt1 , Sost , and Opg were analyzed by real-time quantitative PCR. Data represent the mean ± SD of triplicate samples in representative results from three independent experiments. P < 0.05 vs. control. ns, not significant. Abbreviation: OPG, osteoprotegerin.

Journal: Journal of Dental Sciences

Article Title: Piezo1-mediated mechanotransduction in cementocytes via protein kinase B and p38 mitogen-activated protein kinase signaling

doi: 10.1016/j.jds.2025.08.001

Figure Lengend Snippet: AKT and p38 signaling mediate Yoda1-induced regulation of osteo/cementogenic-related molecules in cementocytes. Cells were pretreated with selective inhibitors of ERK1/2 (PD98059), JNK (JNK inhibitor II), p38 (SB203580), or AKT (AKT inhibitor IV), followed by stimulation with 5 μM Yoda1 for 6 h in the presence of each inhibitor. Expression of Wnt1 , Sost , and Opg were analyzed by real-time quantitative PCR. Data represent the mean ± SD of triplicate samples in representative results from three independent experiments. P < 0.05 vs. control. ns, not significant. Abbreviation: OPG, osteoprotegerin.

Article Snippet: Primary antibodies (Cell Signaling) included phospho/total p38 MAPK (1:1000), phospho-AKT (1:2000), and total AKT (1:1000).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Control

Cyclic stretch induces phosphorylation of AKT and p38 in cementocytes. Cells were subjected to cyclic stretch at 10 % elongation (10 cycles/min) for 10, 30, 60, or 180 min. Phosphorylation levels of AKT and p38 MAPK were analyzed by Western blotting using anti-phospho-AKT, anti-AKT, anti-phospho-p38 MAPK, and anti-p38 MAPK antibodies. Protein sizes: phospho-AKT and AKT (60 kDa); phospho-p38 MAPK (43 kDa) and p38 MAPK (40 kDa). Representative immunoblots and quantification graphs from three independent experiments are shown. P < 0.05 vs. control. ns, not significant.

Journal: Journal of Dental Sciences

Article Title: Piezo1-mediated mechanotransduction in cementocytes via protein kinase B and p38 mitogen-activated protein kinase signaling

doi: 10.1016/j.jds.2025.08.001

Figure Lengend Snippet: Cyclic stretch induces phosphorylation of AKT and p38 in cementocytes. Cells were subjected to cyclic stretch at 10 % elongation (10 cycles/min) for 10, 30, 60, or 180 min. Phosphorylation levels of AKT and p38 MAPK were analyzed by Western blotting using anti-phospho-AKT, anti-AKT, anti-phospho-p38 MAPK, and anti-p38 MAPK antibodies. Protein sizes: phospho-AKT and AKT (60 kDa); phospho-p38 MAPK (43 kDa) and p38 MAPK (40 kDa). Representative immunoblots and quantification graphs from three independent experiments are shown. P < 0.05 vs. control. ns, not significant.

Article Snippet: Primary antibodies (Cell Signaling) included phospho/total p38 MAPK (1:1000), phospho-AKT (1:2000), and total AKT (1:1000).

Techniques: Phospho-proteomics, Western Blot, Control

Vascular density and development in wt versus Tab1 KI mice after OIR. (A) Schematic model of Tab1 KI mice showing the four‐point mutation blocking Tab1 interaction and atypical p38 signaling. (B) Timeline of OIR injury to mice from pn0 to pn17. (C) Retinal flat mounts of room air wt (i) and Tab1 KI (ii) mice with vasculature stained by Isolectin B4 (red). (D) Retinal flat mounts of OIR wt (i) and Tab1 KI (ii) mice with vasculature stained by Isolectin‐B4 (red). (E) Sholl analysis graph of blood vessel density in OIR wt and Tab1 KI mice at radii of 1–1000 pixels from optic nerve (OIR n = 6, RA n = 4). Room air samples are underlaid behind OIR samples and shaded for comparison. Significant values are displayed in Table . (F) Retinal flat mount of pn17 wt (i) and Tab1 KI (ii) mice showing avascular area (dashed outline) and neovascular tufts (white dots). Scale bar = 500 μm. (G–L) Quantification of the (G) avascular area, (H) tuft area, (I) tuft size, (J) vascular length, (K) branch points, and (L) endpoints in wt and Tab1 KI mice, each retina marked as a single data point. n ≥ 13, were analyzed by t ‐test (**** p < 0.0001).

Journal: The FASEB Journal

Article Title: Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery

doi: 10.1096/fj.202503114R

Figure Lengend Snippet: Vascular density and development in wt versus Tab1 KI mice after OIR. (A) Schematic model of Tab1 KI mice showing the four‐point mutation blocking Tab1 interaction and atypical p38 signaling. (B) Timeline of OIR injury to mice from pn0 to pn17. (C) Retinal flat mounts of room air wt (i) and Tab1 KI (ii) mice with vasculature stained by Isolectin B4 (red). (D) Retinal flat mounts of OIR wt (i) and Tab1 KI (ii) mice with vasculature stained by Isolectin‐B4 (red). (E) Sholl analysis graph of blood vessel density in OIR wt and Tab1 KI mice at radii of 1–1000 pixels from optic nerve (OIR n = 6, RA n = 4). Room air samples are underlaid behind OIR samples and shaded for comparison. Significant values are displayed in Table . (F) Retinal flat mount of pn17 wt (i) and Tab1 KI (ii) mice showing avascular area (dashed outline) and neovascular tufts (white dots). Scale bar = 500 μm. (G–L) Quantification of the (G) avascular area, (H) tuft area, (I) tuft size, (J) vascular length, (K) branch points, and (L) endpoints in wt and Tab1 KI mice, each retina marked as a single data point. n ≥ 13, were analyzed by t ‐test (**** p < 0.0001).

Article Snippet: The following antibodies were used: Rabbit anti‐GFAP (DAKO, #Z0334), Mouse anti‐CD31 (DAKO, #M0823), Rabbit anti‐glutamate synthase (Abcam, #ab228590), Rabbit anti‐Iba1 (WAKO, #019‐19741), Isolectin‐B4 Alexa‐Fluor 488 (Invitrogen, # I21411 ), Mouse anti‐VEGFA (Santa Cruz, #SC‐7269), Rabbit total p38 (Cell Signaling Technologies, #9212S), Rabbit phospho‐p38 (Cell Signaling Technologies, #4511S), Mouse anti‐Tab1 (Gentex, #GTX107571), Rabbit anti‐phospho‐MKK3/6 (Cell Signaling Technologies, #9231S), and Rabbit anti‐total‐MKK6 (Cell Signaling Technologies, #8550S), Donkey anti‐Rabbit IgG Alexa Fluor 488 (Invitrogen, # A‐20216), Donkey anti‐Mouse IgG (H + L) Alexa Fluor 555 (Invitrogen, #A‐31570), Goat anti‐rabbit IgG (H + L)‐HRP Conjugate (Bio‐Rad Laboratories, 1 706 515), Goat anti‐mouse IgG (H + L)‐HRP Conjugate (Bio‐Rad Laboratories, #1706516), and PhosTag (Wako Pure Chemical Industries, #AAL‐107).

Techniques: Mutagenesis, Blocking Assay, Staining, Comparison

P38 activity in wt and Tab1 KI retinae. RNAseq analysis of wt or Tab1 KI retinae, from pn17 RA or pn17 OIR mice. (A) A schematic flowchart illustrating distinct data explored: TF's and mRNA signatures associated with wt or tab1 KI retinae. (B) Comparison of GSEA‐published p38 gene expression barcodes. (C) Venn diagram of overlapping genes comparing wt and Tab1 KI retinae from pn17 OIR mice. (D) Example Biocarta p38 signaling gene set, graphing of Z ‐score comparisons between RA, OIR, wt, and Tab1 KI retinae. (E) Immunoblotting of RA, OIR, wt and Tab1 KI retinae, anti‐phospho‐p38, anti‐p38, anti‐phospho‐MKK3/6, anti‐MKK3, anti‐MKK6, anti‐Tab1 PhosTAG, anti‐Tab1, and anti‐phospho‐MK2. Anti‐MK2 (F–H) quantification of immunoblots from retinae. (F) Fold change of phospho‐p38 over total p38 quantified, mean ± SD, ( n = 5). (G) Fold change of phospho‐MKK3/6 over total MKK6 quantified, mean ± SD, ( n = 5). (H) Fold change of phospho‐MK2 over total MK2 quantified, mean ± SD, ( n = 5). (I, J) Representative immunoblot of HREC cells and stimulated with 10 μM PGE 2 (I) or 1 μM histamine (J) for the indicated times in the presence of p38 inhibitor 10 μM SB203580 or DMSO control. (K, L) Fold change of phospho‐p38 over total p38 quantified from three independent repeats, for PGE 2 (K) or histamine (L) (mean ± SD). All immunoblots were analyzed by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: The FASEB Journal

Article Title: Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery

doi: 10.1096/fj.202503114R

Figure Lengend Snippet: P38 activity in wt and Tab1 KI retinae. RNAseq analysis of wt or Tab1 KI retinae, from pn17 RA or pn17 OIR mice. (A) A schematic flowchart illustrating distinct data explored: TF's and mRNA signatures associated with wt or tab1 KI retinae. (B) Comparison of GSEA‐published p38 gene expression barcodes. (C) Venn diagram of overlapping genes comparing wt and Tab1 KI retinae from pn17 OIR mice. (D) Example Biocarta p38 signaling gene set, graphing of Z ‐score comparisons between RA, OIR, wt, and Tab1 KI retinae. (E) Immunoblotting of RA, OIR, wt and Tab1 KI retinae, anti‐phospho‐p38, anti‐p38, anti‐phospho‐MKK3/6, anti‐MKK3, anti‐MKK6, anti‐Tab1 PhosTAG, anti‐Tab1, and anti‐phospho‐MK2. Anti‐MK2 (F–H) quantification of immunoblots from retinae. (F) Fold change of phospho‐p38 over total p38 quantified, mean ± SD, ( n = 5). (G) Fold change of phospho‐MKK3/6 over total MKK6 quantified, mean ± SD, ( n = 5). (H) Fold change of phospho‐MK2 over total MK2 quantified, mean ± SD, ( n = 5). (I, J) Representative immunoblot of HREC cells and stimulated with 10 μM PGE 2 (I) or 1 μM histamine (J) for the indicated times in the presence of p38 inhibitor 10 μM SB203580 or DMSO control. (K, L) Fold change of phospho‐p38 over total p38 quantified from three independent repeats, for PGE 2 (K) or histamine (L) (mean ± SD). All immunoblots were analyzed by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Techniques: Activity Assay, Comparison, Gene Expression, Western Blot, Control

Atypical p38 suppression in the Tab1 KI OIR significantly changes p38‐dependent transcriptional outcomes. RNAseq analysis of wt or Tab1 KI retinae, from pn17 RA or pn17 OIR mice. (A) Z ‐score heatmap for genes with higher expression in wt OIR than Tab1 KI OIR retinae. (B) Example genes from Biocarta p38 signaling gene set, graphing of Z ‐score comparisons between RA, OIR, wt, and Tab1 KI retinae, where there is an increase in wt OIR relative to RA, but downregulation in Tab1KI OIR retinae. (C) A schematic flowchart illustrating distinct data explored: TF's and mRNA signatures associated with p38 activation. (D) Z ‐score heatmap for activity of TF's known to be downstream of p38. (E) Z ‐score, relative expression of p38‐regulated TFs from (D). (F) Z ‐score, relative expression of Mef2A, (G) Z ‐score, relative expression of Mef2C. (H) Z ‐score heatmap for the activity of a selection of top TF's not directly linked to p38, for each experimental condition. Analyzed by one‐way ANOVA (* p < 0.05, ** p < 0.01, **** p < 0.0001).

Journal: The FASEB Journal

Article Title: Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery

doi: 10.1096/fj.202503114R

Figure Lengend Snippet: Atypical p38 suppression in the Tab1 KI OIR significantly changes p38‐dependent transcriptional outcomes. RNAseq analysis of wt or Tab1 KI retinae, from pn17 RA or pn17 OIR mice. (A) Z ‐score heatmap for genes with higher expression in wt OIR than Tab1 KI OIR retinae. (B) Example genes from Biocarta p38 signaling gene set, graphing of Z ‐score comparisons between RA, OIR, wt, and Tab1 KI retinae, where there is an increase in wt OIR relative to RA, but downregulation in Tab1KI OIR retinae. (C) A schematic flowchart illustrating distinct data explored: TF's and mRNA signatures associated with p38 activation. (D) Z ‐score heatmap for activity of TF's known to be downstream of p38. (E) Z ‐score, relative expression of p38‐regulated TFs from (D). (F) Z ‐score, relative expression of Mef2A, (G) Z ‐score, relative expression of Mef2C. (H) Z ‐score heatmap for the activity of a selection of top TF's not directly linked to p38, for each experimental condition. Analyzed by one‐way ANOVA (* p < 0.05, ** p < 0.01, **** p < 0.0001).

Techniques: Expressing, Activation Assay, Activity Assay, Selection

Transcriptomic and pathway insights into zebrafish brain regeneration. A ) Gene Ontology (GO) enrichment analysis of biological processes (BP), molecular functions (MF), and cellular components (CC) across the three regenerative stages (1, 4, and 7 days post-lesion; dpl). The vertical axis lists the enriched GO terms, while the horizontal bars represent the gene ratios associated with each term. The depth of the color indicates the adjusted p-value, and the circle size corresponds to gene counts contributing to each term. B ) heatmap showing the expression levels of key cell cycle-related genes at 1, 4, and 7 dpl. Stage-specific activation patterns, such as peak expression of proliferation markers (aurka, aurkb, wdr76, etc.) at 4 dpl and sustained expression of MCM proteins, reflect dynamic cellular processes during brain regeneration. C ) overview of KEGG pathways enriched across the three regeneration stages. The visualization underscores the pathways driving key biological processes during zebrafish brain regeneration. D ) heatmaps showing the expression of genes related to the MAPK signaling pathway: i ) upregulated genes and ii ) downregulated genes, across the three stages, emphasizing the dynamic regulation of this critical pathway. E ) immunoblot analysis showing the levels of phosphorylated (active) and total p38α MAPK protein during zebrafish brain regeneration. F ) immunoblot analysis showing the levels of phosphorylated (active) and total MK2 and Hsp27 along with c-Jun protein during zebrafish brain regeneration. β-actin was used as the loading control for both E-F panels. G ) quantification of phosphorylated (active) and total p38α MAPK levels during regeneration is shown as a bar graph ( n = 3). H ) quantification of phosphorylated (active) and total MK2 levels during regeneration is shown as a bar graph ( n = 3). I ) quantification of c-Jun levels during regeneration is shown as a bar graph ( n = 3). J ) quantification of phosphorylated (active) and total HSP27 levels during regeneration is shown as a bar graph ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. dpl: days post-lesion

Journal: Journal of Translational Medicine

Article Title: From injury to recovery: transcriptomic dynamics in zebrafish brain regeneration

doi: 10.1186/s12967-025-07400-7

Figure Lengend Snippet: Transcriptomic and pathway insights into zebrafish brain regeneration. A ) Gene Ontology (GO) enrichment analysis of biological processes (BP), molecular functions (MF), and cellular components (CC) across the three regenerative stages (1, 4, and 7 days post-lesion; dpl). The vertical axis lists the enriched GO terms, while the horizontal bars represent the gene ratios associated with each term. The depth of the color indicates the adjusted p-value, and the circle size corresponds to gene counts contributing to each term. B ) heatmap showing the expression levels of key cell cycle-related genes at 1, 4, and 7 dpl. Stage-specific activation patterns, such as peak expression of proliferation markers (aurka, aurkb, wdr76, etc.) at 4 dpl and sustained expression of MCM proteins, reflect dynamic cellular processes during brain regeneration. C ) overview of KEGG pathways enriched across the three regeneration stages. The visualization underscores the pathways driving key biological processes during zebrafish brain regeneration. D ) heatmaps showing the expression of genes related to the MAPK signaling pathway: i ) upregulated genes and ii ) downregulated genes, across the three stages, emphasizing the dynamic regulation of this critical pathway. E ) immunoblot analysis showing the levels of phosphorylated (active) and total p38α MAPK protein during zebrafish brain regeneration. F ) immunoblot analysis showing the levels of phosphorylated (active) and total MK2 and Hsp27 along with c-Jun protein during zebrafish brain regeneration. β-actin was used as the loading control for both E-F panels. G ) quantification of phosphorylated (active) and total p38α MAPK levels during regeneration is shown as a bar graph ( n = 3). H ) quantification of phosphorylated (active) and total MK2 levels during regeneration is shown as a bar graph ( n = 3). I ) quantification of c-Jun levels during regeneration is shown as a bar graph ( n = 3). J ) quantification of phosphorylated (active) and total HSP27 levels during regeneration is shown as a bar graph ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. dpl: days post-lesion

Article Snippet: Rabbit monoclonal Phospho p38 MAPK (1:1000; 4511S; Cell Signaling Technology), rabbit polyclonal total p38 MAPK (1:1000; 9212S; Cell Signaling Technology), rabbit monoclonal Phospho HSP27 (1:1000; 9709S; Cell Signaling Technology), mouse monoclonal Total HSP27 (1:500; CPTC-HSPB1-2; Developmental Studies Hybridoma Bank), rabbit monoclonal Phospho MK2 (1:1000; 3007S; Cell Signaling Technology), Total MK2 (1:1000; EB11929; Everest Biotech), rabbit monoclonal c-Jun (1:1000; 9165S; Cell Signaling Technology), mouse monoclonal β-catenin (1:1000; 610153; BD Biosciences), Phospho AKT (1:1000; 4058S; Cell Signaling Technology), Total AKT (1:1000; 2920S; Cell Signaling Technology), mouse monoclonal β-actin (1:1000; sc47778; Santa Cruz).

Techniques: Expressing, Activation Assay, Western Blot, Control

BIRB796-mediated inhibition of MAPK14a pathway impairs the regenerative response post traumatic brain injury. A ) schematic showing BIRB796 treatment after zebrafish brain injury and the brains harvested at 4 dpl. Treatment regimen: animals were immersed in system water containing 0.5 μM or 1 μM BIRB796 (or vehicle control: 0.1% DMSO) immediately after lesion induction and maintained until sacrifice at 4 dpl. B ) immunoblot analysis showing the levels of phosphorylated (active) and total p38α MAPK protein upon BIRB796 treatment at 4 dpl;. *represents the band for p38α MAPK. C ) quantification of phosphorylated (active) and total p38α MAPK levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). D ) immunoblot analysis showing the levels of phosphorylated (active) and total Hsp27 protein upon BIRB796 treatment at 4 dpl E ) quantification of phosphorylated (active) and total Hsp27 levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). F ) immunoblot analysis showing the levels of phosphorylated (active) and total MK2 and c-Jun protein upon BIRB796 treatment at 4 dpl. G ) quantification of phosphorylated (active)and total MK2 levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). H ) quantification of c-Jun levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. ( I ) Immunofluorescence staining on 4 dpl zebrafish brains treated with DMSO (control) or 1 μM BIRB796. Panels show staining with the following markers: PCNA (red), HuC/D (red), GFAP (green), and S100B (green), with DAPI used to label nuclei. ( A - D ) DMSO control, (A’-D’) BIRB796 treatment. Scale bar denotes 10 μm. The following anatomical regions are indicated: Dc (central zone of the dorsal telencephalic area), Dm (medial zone of dorsal telencephalic area), Dl (lateral zone of dorsal telencephalic area), Vd (dorsal nucleus of ventral telencephalic area). ( J - M ) quantification of immunostaining wherein injured hemisphere of 4 dpl regenerating brain has been compared to that of 4 dpl BIRB796 treated regenerating brain ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. cntrl: control; dpl: days post-lesion

Journal: Journal of Translational Medicine

Article Title: From injury to recovery: transcriptomic dynamics in zebrafish brain regeneration

doi: 10.1186/s12967-025-07400-7

Figure Lengend Snippet: BIRB796-mediated inhibition of MAPK14a pathway impairs the regenerative response post traumatic brain injury. A ) schematic showing BIRB796 treatment after zebrafish brain injury and the brains harvested at 4 dpl. Treatment regimen: animals were immersed in system water containing 0.5 μM or 1 μM BIRB796 (or vehicle control: 0.1% DMSO) immediately after lesion induction and maintained until sacrifice at 4 dpl. B ) immunoblot analysis showing the levels of phosphorylated (active) and total p38α MAPK protein upon BIRB796 treatment at 4 dpl;. *represents the band for p38α MAPK. C ) quantification of phosphorylated (active) and total p38α MAPK levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). D ) immunoblot analysis showing the levels of phosphorylated (active) and total Hsp27 protein upon BIRB796 treatment at 4 dpl E ) quantification of phosphorylated (active) and total Hsp27 levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). F ) immunoblot analysis showing the levels of phosphorylated (active) and total MK2 and c-Jun protein upon BIRB796 treatment at 4 dpl. G ) quantification of phosphorylated (active)and total MK2 levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). H ) quantification of c-Jun levels in control regenerating (4 dpl DMSO) brain and BIRB796 treated regenerating (4 dpl) brain is shown as a bar graph ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. ( I ) Immunofluorescence staining on 4 dpl zebrafish brains treated with DMSO (control) or 1 μM BIRB796. Panels show staining with the following markers: PCNA (red), HuC/D (red), GFAP (green), and S100B (green), with DAPI used to label nuclei. ( A - D ) DMSO control, (A’-D’) BIRB796 treatment. Scale bar denotes 10 μm. The following anatomical regions are indicated: Dc (central zone of the dorsal telencephalic area), Dm (medial zone of dorsal telencephalic area), Dl (lateral zone of dorsal telencephalic area), Vd (dorsal nucleus of ventral telencephalic area). ( J - M ) quantification of immunostaining wherein injured hemisphere of 4 dpl regenerating brain has been compared to that of 4 dpl BIRB796 treated regenerating brain ( n = 3). Significance is represented as n.s. for p-value > 0.05, * for p-value < 0.05, ** for p-value < 0.01 and *** for p-value < 0.001. cntrl: control; dpl: days post-lesion

Techniques: Inhibition, Control, Western Blot, Immunofluorescence, Staining, Immunostaining

A. ovPrP Sc -488 uptake upon treatment with 50 ng of BMP peptides added daily to the culture medium for 4 days. B. Western Blot quantification of canonical (pSMAD1/5) and non-canonical (pERK1/2, pAKT, phospho p38/p38) BMP downstream effectors. Vinculin: loading control. Dots: two biological replicates. All samples of each biological replicate were normalized to untreated controls (UT). C. Western Blot quantification of canonical (pSMAD1/5) BMP downstream effectors. Vinculin: loading control. Statistics in all panels: one-way Anova; Dunnett’s post-hoc test.

Journal: bioRxiv

Article Title: The Bone Morphogenetic Pathway Controls the Uptake of Infectious Prions

doi: 10.1101/2025.11.08.687161

Figure Lengend Snippet: A. ovPrP Sc -488 uptake upon treatment with 50 ng of BMP peptides added daily to the culture medium for 4 days. B. Western Blot quantification of canonical (pSMAD1/5) and non-canonical (pERK1/2, pAKT, phospho p38/p38) BMP downstream effectors. Vinculin: loading control. Dots: two biological replicates. All samples of each biological replicate were normalized to untreated controls (UT). C. Western Blot quantification of canonical (pSMAD1/5) BMP downstream effectors. Vinculin: loading control. Statistics in all panels: one-way Anova; Dunnett’s post-hoc test.

Article Snippet: The following antibodies were used: anti-Cas9 1:1000 (Cell Signaling, #14697), anti-actin HRP conjugated 1:10’000 (Sigma-Aldrich, A3854), anti-Rab13 1:1000 (Abcam, ab180936), anti-ADAM10 1:1000 (Abcam, ab124695), anti-vinculin 1:1000 (Abcam, ab129002), anti-PrP POM2 0.3 mg/mL, anti-PrP POM1 0.3 mg/mL, anti phospho SMAD1/5 (CellSignaling #9516), anti pERK1/2 (CellSignaling #4370), anti phospho AKT (CellSignaling #4060), anti phospho p38 MAPK (CellSignaling #9211), anti-total p38 MAPK (CellSignaling #9212), anti-Rabbit-HRP 1:10’000 (Jackson ImmunoResearch #111-035-045), anti-Mouse-HRP 1:10’000 (Jackson ImmunoResearch #115-035-005), anti-Goat-HRP 1:10’000 (Jackson ImmunoResearch #705-035-147).

Techniques: Western Blot, Control

A. Western Blots of canonical (pSMAD1/5) and non-canonical (pERK1/2, pAKT, phosphor p38/p38) downstream effectors of the BMP pathway in SH-KO vp649 cells treated with individual or combinations of BMP peptides at 50 ng/mL for 4 days. UT: untreated control. B. Western Blot of canonical (pSMAD1/5) downstream effector of the BMP pathway in SH-KO vp649 upon genetic upregulation of individual hit genes. Vinculin was used as loading control.

Journal: bioRxiv

Article Title: The Bone Morphogenetic Pathway Controls the Uptake of Infectious Prions

doi: 10.1101/2025.11.08.687161

Figure Lengend Snippet: A. Western Blots of canonical (pSMAD1/5) and non-canonical (pERK1/2, pAKT, phosphor p38/p38) downstream effectors of the BMP pathway in SH-KO vp649 cells treated with individual or combinations of BMP peptides at 50 ng/mL for 4 days. UT: untreated control. B. Western Blot of canonical (pSMAD1/5) downstream effector of the BMP pathway in SH-KO vp649 upon genetic upregulation of individual hit genes. Vinculin was used as loading control.

Techniques: Western Blot, Control

Review

anti total p38 (Cell Signaling Technology Inc)

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