p38 mitogen activated protein kinase mapk  (Cell Signaling Technology Inc)

Journal: World Journal of Gastroenterology

Article Title: Kushenol I combats ulcerative colitis via intestinal barrier preservation and gut microbiota optimization

doi: 10.3748/wjg.v31.i26.105656

Figure Lengend Snippet: Molecular docking and corresponding scores of kushenol I with key targets protein kinase B, p38 mitogen-activated protein kinase, NOD-like receptor thermal protein domain associated protein 3, phosphoinositide 3-kinase, protein kinase B, forkhead box O1, and Toll-like receptor 4, are presented. AKT: Protein kinase B; FOXO1: Forkhead box O1; NF-κB: Nuclear factor kappa B; NLRP3: NOD-like receptor thermal protein domain associated protein 3; p38 MAPK: p38 mitogen-activated protein kinase; PI3K: Phosphoinositide 3-kinase; TLR4: Toll-like receptor 4.

Article Snippet: Antibodies targeting forkhead box O1 (FOXO1), p38 mitogen-activated protein kinase (p38 MAPK), phosphorylated p38 MAPK (p-p38 MAPK), protein kinase B (AKT), phosphorylated protein kinase B (p-AKT), and β-actin were sourced from Proteintech (Proteintech, Rosemont, IL, United States).

Techniques:

Journal: World Journal of Gastroenterology

Article Title: Kushenol I combats ulcerative colitis via intestinal barrier preservation and gut microbiota optimization

doi: 10.3748/wjg.v31.i26.105656

Figure Lengend Snippet: Molecular dynamics simulation results of kushenol I interacting with protein kinase B, forkhead box O1, nuclear factor kappa B, NOD-like receptor thermal protein domain associated protein 3, phosphoinositide 3-kinase, p38 mitogen-activated protein kinase, and Toll-like receptor 4. A: Fluctuation curves of hydrogen bond numbers; B: Radius of gyration curves; C: Root mean square deviation curves; D: Root mean square fluctuation curves; E: Free energy landscape. AKT: Protein kinase B; FOXO1: Forkhead box O1; NF-κB: Nuclear factor kappa B; NLRP3: NOD-like receptor thermal protein domain associated protein 3; p38 MAPK: p38 mitogen-activated protein kinase; PI3K: Phosphoinositide 3-kinase; Rg: Gyration radius; RMSD: Root mean square deviation; RMSF: Root mean square deviation; TLR4: Toll-like receptor 4.

Article Snippet: Antibodies targeting forkhead box O1 (FOXO1), p38 mitogen-activated protein kinase (p38 MAPK), phosphorylated p38 MAPK (p-p38 MAPK), protein kinase B (AKT), phosphorylated protein kinase B (p-AKT), and β-actin were sourced from Proteintech (Proteintech, Rosemont, IL, United States).

Techniques:

Journal: World Journal of Gastroenterology

Article Title: Kushenol I combats ulcerative colitis via intestinal barrier preservation and gut microbiota optimization

doi: 10.3748/wjg.v31.i26.105656

Figure Lengend Snippet: Effects of kushenol I on the expression of inflammation-related proteins phosphorylated phosphoinositide 3-kinase (PI3K), PI3K, phosphorylated protein kinase B (AKT), AKT, forkhead box O1, interleukin 1β, Toll-like receptor 4, phosphorylated p38 mitogen-activated protein kinase (MAPK), p38 MAPK, nuclear factor kappa B phosphorylated p65, nuclear factor kappa B p65, and NOD-like receptor thermal protein domain associated protein 3 in the colonic tissues of mice with ulcerative colitis. A: Image of a gel showing protein expression; B: Bar graph depicting protein expression. Values are presented as the mean ± standard error of the mean ( n = 3). a P < 0.05. b P < 0.01. c P < 0.001. P compared with the model group. AKT: Protein kinase B; FOXO1: Forkhead box O1; IL-1β: Interleukin 1β; PI3K: Phosphoinositide 3-kinase; p-p38: Phosphorylated p38; p38 MAPK: p38 mitogen-activated protein kinase; p-p65: Phosphorylated p65; p-PI3K: Phosphorylated phosphoinositide 3-kinase; p-AKT: Phosphorylated protein kinase B; NF-κB: Nuclear factor kappa B; NLRP3: NOD-like receptor thermal protein domain associated protein 3; TLR4: Toll-like receptor 4.

Article Snippet: Antibodies targeting forkhead box O1 (FOXO1), p38 mitogen-activated protein kinase (p38 MAPK), phosphorylated p38 MAPK (p-p38 MAPK), protein kinase B (AKT), phosphorylated protein kinase B (p-AKT), and β-actin were sourced from Proteintech (Proteintech, Rosemont, IL, United States).

Techniques: Expressing

Journal: Investigative Ophthalmology & Visual Science

Article Title: Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes

doi: 10.1167/iovs.66.6.6

Figure Lengend Snippet: KD of FADS1 activates the MAPK signaling pathway in vitro. ( A , B ) Western blotting analysis of phospho-p38 MAPK and p38 MAPK in HCECs transfected with NC siRNA or FADS1 siRNA ( n = 3). All values are mean ± SEM. ** P < 0.01.

Article Snippet: Equal amounts of protein were separated by SDS-PAGE and immunoblotted with primary antibodies against FADS1 (Santa Cruz), HSP60 (Santa Cruz), GRP75 (Santa Cruz), PAX6 (Abcam), SDHA (Abcam), p38 mitogen-activated protein kinase (MAPK) (Cell Signaling Technology), phospho-p38 MAPK (Cell Signaling Technology), LC3B (Cell Signaling Technology), VDAC (Cell Signaling Technology), P62 (MBL Life Science, Tokyo, Japan), FADS1 (Proteintech, Rosemont, IL, USA), Lamin A/C (Proteintech), TOMM40 (Proteintech), and GAPDH (Proteintech).

Techniques: In Vitro, Western Blot, Transfection

Journal: Investigative Ophthalmology & Visual Science

Article Title: Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes

doi: 10.1167/iovs.66.6.6

Figure Lengend Snippet: FADS1 KD promotes cell migration by increasing the upstream metabolite GLA. ( A ) n-6 PUFA and n-3 PUFA metabolic pathways involving FADS1. ( B , C ) Representative scratch assay images and statistical analysis of wound healing rates for HCECs after transfection with NC siRNA or FADS2 siRNA ( n = 9). ( D , E ) Representative scratch assay images and statistical analysis of wound healing rates for HCECs after transfection with NC siRNA or PTGES siRNA2 ( n = 9). ( F ) Measurement of various fatty acid levels in HCECs transfected with NC siRNA or FADS1 siRNA. ( G ) Quantitative analysis of GLA content ( n = 8). ( H , I ) Representative scratch assay images and statistical analysis of wound healing rates for HCECs treated with GLA (20 µg/mL, 48 h), with DMSO as the control ( n = 9). ( J , K ) Western blotting analysis of phospho-p38 MAPK and p38 MAPK in HCECs after treatment with GLA (20 µg/mL, 48 h), with DMSO as the control ( n = 3). All values are mean ± SEM. ** P < 0.01; **** P < 0.0001; ns, nonsignificant.

Article Snippet: Equal amounts of protein were separated by SDS-PAGE and immunoblotted with primary antibodies against FADS1 (Santa Cruz), HSP60 (Santa Cruz), GRP75 (Santa Cruz), PAX6 (Abcam), SDHA (Abcam), p38 mitogen-activated protein kinase (MAPK) (Cell Signaling Technology), phospho-p38 MAPK (Cell Signaling Technology), LC3B (Cell Signaling Technology), VDAC (Cell Signaling Technology), P62 (MBL Life Science, Tokyo, Japan), FADS1 (Proteintech, Rosemont, IL, USA), Lamin A/C (Proteintech), TOMM40 (Proteintech), and GAPDH (Proteintech).

Techniques: Migration, Wound Healing Assay, Transfection, Control, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Hydrogen sulfide and ferroptosis inhibition underlies the dietary restriction-induced protection against cyclophosphamide cystitis

doi: 10.3389/fphar.2025.1562852

Figure Lengend Snippet: NaHS and DATS protect against ACR-induced urothelial cell injury. (A,B) Effect of DATS on H 2 S production capacity in urothelial cells. SV-HUC-1 cells treated with indicated concentrations of DATS were subjected to lead sulfide assay for 24 h (A) . Densitometric quantification of the intensity of the colored circles was performed, and data shown in (B) have been normalized to control (mean ± S.E.; n = 5; ** P < 0.01). (C,D) Effect of NaHS and DATS on ACR-induced urothelial cell death. SV-HUC-1 cells were pretreated with 1 mM NaHS for 15 min or 25 μM DATS for 30 min before exposing to 100 μM ACR for an additional 24 h. The cell viability was determined by Calcein-AM/PI staining (upper) and WST assay (lower). Data shown are mean ± S.E. (n = 5 and 6, respectively; ** P < 0.01). (E,F) Effect of NaHS and DATS on ACR-induced oxidative stress in urothelial cells. SV-HUC-1 cells were pretreated with 1 mM NaHS for 15 min or 25 μM DATS for 30 min before exposing to 75 μM ACR for an additional 4 h. Cell proteins were extracted for Western blot analysis of protein carbonylation and phosphorylated P38MAPK. A quantitative analysis of blots is shown below. Data are presented as mean ± S.E. (n = 3; * P < 0.05, ** P < 0.01).

Article Snippet: Antibodies against γ-H2A.X (#9718), GPX4 (#52455), phospho-p38 mitogen activated protein kinase (Thr180/Tyr182) (p-P38MAPK, #8203S), α-tubulin (#3873T), rabbit IgG (#5366), and mouse IgG (#5470) were from Cell Signaling Technology (Danvers, MA, United States).

Techniques: Control, Staining, WST Assay, Western Blot

Journal: bioRxiv

Article Title: Acute session of three endurance exercise intensities alters subcutaneous adipose tissue transcriptome in regular exercisers

doi: 10.1101/2025.05.02.651890

Figure Lengend Snippet: A) Ratio of pERK T202/Y204 :ERK. B) Ratio of pP38 T180/Y182 :P38. C) Ratio of pSTAT3 Y705 :STAT3. D) Ratio of pHSL S565 :HSL and pHSL S660 :HSL. E) Ratio of pAKT T308 :AKT and pAKT S473 :AKT. *p<0.05 vs. Pre. There was no significant Time x Group interaction effect. Data is presented as Mean±SD.

Article Snippet: Primary antibodies used were Hormone-sensitive lipase (HSL, #18381, Cell Signaling Technology), phospho-HSL (Ser565) (pHSL S565 , #4137, Cell Signaling Technology), phospho-HSL (Ser660) (pHSL S660 , #4126, Cell Signaling Technology), Protein kinase B (AKT, #9272, Cell Signaling Technology), phospho-AKT (Ser473) (pAKT S473 , #9271, Cell Signaling Technology), phospho-AKT (Thr308) (pAKT T308 , #13038, Cell Signaling Technology), p38 mitogen-activated protein kinase (P38, #9212, Cell Signaling Technology), phospho-P38 MAPK (Thr180/Tyr182) (pP38 T180/Y192 , #9211, Cell Signaling Technology), p44/42 MAPK extracellular signal-regulated kinase (ERK, #4695, Cell Signaling Technology), phospho-p44/42 MAPK (Thr202/Tyr204) (pERK T202/Y204 , #4376, Cell Signaling Technology), Signal transducer and activator of transcription 3 (STAT3, #12640, Cell Signaling Technology), and phospho-STAT3 (Tyr705) (pSTAT3 Y705 , #9145, Cell Signaling Technology).

Techniques: