p38 mapk pathway (MedChemExpress)

MedChemExpress is a verified supplier

MedChemExpress manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

MedChemExpress p38 mapk pathway

Oba inhibits the <t>TLR4/MyD88/p38</t> MAPK signaling pathway in both in vivo and in vitro experiments. ( A – D ) Molecular docking analysis of Oba with TLR4. ( E – H ) Molecular docking analysis of Oba with MyD88. ( I – L ) Molecular docking analysis of Oba with p38. For each protein, the analysis is presented as: an overall docking pose with the binding region outlined by a red dashed box ( A, E, I ); a close-up view of the binding region ( B, F, J ); a surface representation ( C, G, K ); and a two-dimensional interaction diagram ( D, H, L ). ( M ) Representative Western blot image of TLR4, MyD88, p-p38 and p38 protein in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: LPS, and 50 μM Oba. ( N ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in BV-2 cells (n = 5). ( O ) Western blot analysis of TLR4, MyD88, p-p38, and p38 in spinal cord tissues from Sham, SCI, and SCI + Oba (20 mg/kg) groups at 3 days post-SCI. ( P ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in spinal cord tissues (n = 5). The values are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001; NS, not significant.

P38 Mapk Pathway, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p38+mapk+pathway/Phospho-p38+alpha%2FMAPK14+(Thr180%2BTyr182)+Antibody/pmc12994538-112-6-34
Average 97 stars, based on 162 article reviews

p38 mapk pathway - by Bioz Stars, 2026-09

97/100 stars

Images

1) Product Images from "Obacunone Promotes Functional Recovery After Spinal Cord Injury by Attenuating Neuroinflammation by Targeting the TLR4/MyD88/p38 MAPK Pathway"

Article Title: Obacunone Promotes Functional Recovery After Spinal Cord Injury by Attenuating Neuroinflammation by Targeting the TLR4/MyD88/p38 MAPK Pathway

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S577707

Oba inhibits the TLR4/MyD88/p38 MAPK signaling pathway in both in vivo and in vitro experiments. ( A – D ) Molecular docking analysis of Oba with TLR4. ( E – H ) Molecular docking analysis of Oba with MyD88. ( I – L ) Molecular docking analysis of Oba with p38. For each protein, the analysis is presented as: an overall docking pose with the binding region outlined by a red dashed box ( A, E, I ); a close-up view of the binding region ( B, F, J ); a surface representation ( C, G, K ); and a two-dimensional interaction diagram ( D, H, L ). ( M ) Representative Western blot image of TLR4, MyD88, p-p38 and p38 protein in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: LPS, and 50 μM Oba. ( N ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in BV-2 cells (n = 5). ( O ) Western blot analysis of TLR4, MyD88, p-p38, and p38 in spinal cord tissues from Sham, SCI, and SCI + Oba (20 mg/kg) groups at 3 days post-SCI. ( P ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in spinal cord tissues (n = 5). The values are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001; NS, not significant.

Figure Legend Snippet: Oba inhibits the TLR4/MyD88/p38 MAPK signaling pathway in both in vivo and in vitro experiments. ( A – D ) Molecular docking analysis of Oba with TLR4. ( E – H ) Molecular docking analysis of Oba with MyD88. ( I – L ) Molecular docking analysis of Oba with p38. For each protein, the analysis is presented as: an overall docking pose with the binding region outlined by a red dashed box ( A, E, I ); a close-up view of the binding region ( B, F, J ); a surface representation ( C, G, K ); and a two-dimensional interaction diagram ( D, H, L ). ( M ) Representative Western blot image of TLR4, MyD88, p-p38 and p38 protein in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: LPS, and 50 μM Oba. ( N ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in BV-2 cells (n = 5). ( O ) Western blot analysis of TLR4, MyD88, p-p38, and p38 in spinal cord tissues from Sham, SCI, and SCI + Oba (20 mg/kg) groups at 3 days post-SCI. ( P ) Quantitative analysis of TLR4 and MyD88 protein levels and p38 phosphorylation in spinal cord tissues (n = 5). The values are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001; NS, not significant.

Techniques Used: In Vivo, In Vitro, Binding Assay, Western Blot, Phospho-proteomics

Oba attenuates inflammation by targeting the TLR4/MyD88/p38 MAPK pathway in BV-2 microglial cells. ( A ) Representative Western blot of TLR4 expression in BV-2 cells transfected with a TLR4 overexpression plasmid (pcDNA3.1-TLR4) or an empty vector. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: empty plasmid (Oe-NC), and TLR4 overexpression plasmid (Oe-TLR4). ( B ) Quantitative analysis of TLR4 protein levels (n = 5). ( C ) Western blot images of iNOS, TLR4, TNFα and IL-1β protein expression in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following treatments in culture: Oe-NC, Oe-TLR4, LPS, and Oba. ( D – G ) Quantitative analysis of iNOS, TLR4, TNFα and IL-1β protein levels (n = 5). ( H ) Representative Western blot images of iNOS, TNFα, IL-1β, p-p38 and p38 in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: LPS, Oba, and SB203580. ( I – L ) Quantitative analysis of iNOS, TNFα, IL-1β protein levels and p38 phosphorylation (n = 5). The values are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001; NS, not significant.

Figure Legend Snippet: Oba attenuates inflammation by targeting the TLR4/MyD88/p38 MAPK pathway in BV-2 microglial cells. ( A ) Representative Western blot of TLR4 expression in BV-2 cells transfected with a TLR4 overexpression plasmid (pcDNA3.1-TLR4) or an empty vector. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: empty plasmid (Oe-NC), and TLR4 overexpression plasmid (Oe-TLR4). ( B ) Quantitative analysis of TLR4 protein levels (n = 5). ( C ) Western blot images of iNOS, TLR4, TNFα and IL-1β protein expression in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following treatments in culture: Oe-NC, Oe-TLR4, LPS, and Oba. ( D – G ) Quantitative analysis of iNOS, TLR4, TNFα and IL-1β protein levels (n = 5). ( H ) Representative Western blot images of iNOS, TNFα, IL-1β, p-p38 and p38 in BV-2 cells. The plus and minus signs (+, -) denote the presence or absence of the following reagents in culture: LPS, Oba, and SB203580. ( I – L ) Quantitative analysis of iNOS, TNFα, IL-1β protein levels and p38 phosphorylation (n = 5). The values are presented as mean ± SD. *p<0.05, **p<0.01, ***p<0.001; NS, not significant.

Techniques Used: Western Blot, Expressing, Transfection, Over Expression, Plasmid Preparation, Phospho-proteomics

Incubation:

Article Title: GDF11 Regulates M1 and M2 Polarization of BV2 Microglial Cells via p38 MAPK Signaling Pathway.
Article Snippet: Growth differentiation factor 11 (GDF11), a member of the transforming growth factor β (TGF-β) superfamily, exhibits great neurological and mental diseases modulating potential.. However, its specific effects on microglia, which are the primary immune cells of the nervous system, remain unclear.. To investigate the mechanism by which GDF11 affects BV2 microglial cells in vitro and to elucidate its regulatory mechanisms, we carried out a systematic examination of how GDF11 affects the various functions of lipopolysaccharide (LPS)-induced BV2 microglial cells and found that endogenous GDF11 could significantly inhibit cell proliferation, apoptosis, and migration.

Injection:

Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia.
Article Snippet: To inhibit p38 MAPK activation, the specific inhibitor SB239063 (10 mg/kg; HY-11068; purity: 99.61%; MedChem Express) was administered intraperitoneally once daily for 7 days. .. Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation19, once daily for 7 days. ..

Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia
Article Snippet: To inhibit p38 MAPK activation, the specific inhibitor SB239063 (10 mg/kg; HY-11068; purity: 99.61%; MedChem Express) was administered intraperitoneally once daily for 7 days. .. Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days. ..

Phospho-proteomics:

other:

Article Title: LncRNA-ATB promotes TGF-β-induced glioma cells invasion through NF-κB and P38/MAPK pathway.
Article Snippet: Funding information Nova Pew Plan of the Second Affiliated Hospital of Anhui Medical University, Grant/ Award Number: 2017KA01; Academic Funding Project for Top Talents in Colleges and Universities in Anhui Province, Grant/ Award Number: gxbjZD10; Natural Science Foundation of Anhui Province, Grant/Award Number: 1608085MH225; National Natural Science Foundation of China, Grant/Award Number: 81502149; Key Research and Development Plan Project of Anhui Province, Grant/Award Number: 1804h08020270 Abstract Glioma constitutes the most aggressive primary intracranial malignancy in adults.. We previously showed that long noncoding RNA activated by TGF‐β (lncRNA‐ATB) promoted the glioma cells invasion.. However, whether lncRNA‐ATB is involved in TGF‐β‐mediated invasion of glioma cells remains unknown.

Western Blot:

Article Title: Nonstructural protein 14 of PDCoV promotes complement C3 expression via the activation of p38-MAPK-C/EBP pathway.
Article Snippet: Porcine deltacoronavirus (PDCoV) is an emergent enteric coronavirus, primarily inducing diarrhea in swine, particularly in nursing piglets, with the additional potential for zoonotic transmission to humans.. Despite the significant impact of PDCoV on swine populations, its pathogenic mechanisms remain incompletely understood.. Complement component 3 (C3) plays a pivotal role in the prevention of viral infections, however, there are no reports concerning the influence of C3 on the proliferation of PDCoV.

Real-time Polymerase Chain Reaction:

Enzyme-linked Immunosorbent Assay:

Expressing:

Infection:

Cell Culture:

Article Title: Nicotinamide mononucleotide and nicotinamide riboside attenuate cytokine production in human keratinocytes via suppression of p38 Pathway
Article Snippet: .. HaCaT cells were seeded in 6-well plates and cultured for 24 h. Cells were pretreated with NMN (0.5, 1, 5 mM) or NR (0.5, 1, 2 mM) for 1 h, then stimulated with TNF-α/IFN-γ (10 ng/mL) for 1 h. To examine the involvement of the p38 MAPK pathway, HaCaT cells were pretreated with 10 μM p38 MAPK inhibitor SB203580 (MedChemExpress, NJ, USA) for 2 h, followed by NMN or NR treatment for 1 h and subsequent stimulation with TNF-α/IFN-γ (10 ng/mL) for 1 h. After washing with cold PBS, cells were lysed in RIPA buffer (Sigma) containing protease and phosphatase inhibitors (Roche). .. Samples were denatured at 95 °C for 5 min, separated by SDS-PAGE, and transferred to PVDF membranes (Millipore).

Blocking Assay:

Article Title: DRD4 alleviates acute kidney injury by suppressing ISG15/NOX4 axis-associated oxidative stress
Article Snippet: Prior to subjecting the cells to H/R or cisplatin treatment, HK-2 cells were incubated with DRD4 agonist PD168077 (10 nM; MCE, Shanghai, China) for 12 h to activate DRD4. .. SB202190 (10 μM; MCE, Shanghai, China) was used to block P38 MAPK pathway. ..

Review