AFfirm™ p38 MAPK Monoclonal Antibody - #BF8015

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产品: p38 MAPK 单克隆 抗体
货号: BF8015
描述: Mouse monoclonal antibody to p38 MAPK
应用: WB IHC
文献验证: WB, IHC
反应: Human, Mouse, Rat
蛋白号: Q16539

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 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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产品描述

来源:
Mouse
应用:
WB 1:1000-1:10000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Monoclonal [AFfirm8015]
特异性:
p38 MAPK Antibody detects endogenous levels of p38 MAPK .
偶联:
Unconjugated.
纯化:
Affinity-chromatography.
保存:
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

CSAID Binding Protein 1; CSAID binding protein; CSAID-binding protein; Csaids binding protein; CSBP 1; CSBP 2; CSBP; CSBP1; CSBP2; CSPB1; Cytokine suppressive anti-inflammatory drug-binding protein; EXIP; MAP kinase 14; MAP kinase MXI2; MAP kinase p38 alpha; MAPK 14; MAPK14; MAX interacting protein 2; MAX-interacting protein 2; Mitogen Activated Protein Kinase 14; Mitogen activated protein kinase p38 alpha; Mitogen-activated protein kinase 14; Mitogen-activated protein kinase p38 alpha; MK14_HUMAN; Mxi 2; MXI2; p38 ALPHA; p38; p38 MAP kinase; p38 MAPK; p38 mitogen activated protein kinase; p38ALPHA; p38alpha Exip; PRKM14; PRKM15; RK; SAPK2A;

抗原和靶标

免疫原:

A synthesized peptide derived from human p38 MAPK.

基因/基因ID:
MAPK14(1432)

研究领域

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Organismal Systems > Circulatory system > Adrenergic signaling in cardiomyocytes.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Platelet activation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc epsilon RI signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Leukocyte transendothelial migration.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Retrograde endocannabinoid signaling.   (View pathway)

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)

· Organismal Systems > Endocrine system > Progesterone-mediated oocyte maturation.

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

文献引用

1). Activation of GPR81 by lactate drives tumour-induced cachexia. Nature metabolism, 2024 (PubMed: 38499763) [IF=20.8]

Application: WB    Species: mice    Sample:

Fig. 5: GPR81 induces WAT browning through activation of p38. a, Heat map showing the differentially phosphorylated proteins and the enriched pathways in the iWAT from WT tumour-free (WT control), WT TB, GPR81 knockout tumour-free (GPR81−/− control) and GPR81−/− tumour-bearing (GPR81−/− TB) mice. b, Result of Kinase–Substrate Enrichment Analysis (KSEA) showing changes in kinase activity in the iWAT of tumour-bearing mice due to GPR81 ablation. Delta counts indicate the number of substrates of each kinase in the iWAT of GPR81−/− TB minus that in the WT TB mice. c, Representative western blots and statistical data showing the levels of phosphorylated (p-p38) and total p38 in the iWAT (n = 6 for each group). d,e, Representative images (d) and statistical data (e) of immunofluorescence signal intensity of p38 (green) and phosphorylated p38 (p-p38; red) in the adipose tissue from patients with or without cancer cachexia (n = 4 for each group). The nuclei were stained with DAPI (blue). Scale bars, 100 μm. f, Representative western blots and statistical data showing the levels of phosphorylated (p-p38), total p38 and UCP1 in the SVF-derived adipocytes treated with sodium l-lactate for the indicated time points (n = 6 biologically independent samples in each group). g, Representative western blots and statistical data showing the lactate-induced activation of p38-ATF2 was abolished in GPR81−/− SVF-derived adipocytes (n = 5 biologically independent samples in each group). h, Knocking down the expression of p38 by specific siRNA abolished the lactate-induced activation of p38-ATF2 and upregulation of UCP1 (n = 5 biologically independent samples in each group). All data are presented as the mean ± s.e.m. P values were determined by one-way ANOVA with Tukey’s multiple-comparisons test (c and f–h) and two-tailed unpaired Student’s t-test (e). In b, KSEA was used to analyze the possible kinases of the differentially phosphorylated peptides and the statistical significance was calculated by hypergeometric test; *p < 0.05, ** p < 0.01.
2). Ly6G+ Neutrophils and Interleukin-17 Are Essential in Protection against Rodent Malaria Caused by Plasmodium berghei ANKA. Research (Washington, D.C.), 2024 (PubMed: 39703777) [IF=11.0]
3). Cetuximab promotes RSL3-induced ferroptosis by suppressing the Nrf2/HO-1 signalling pathway in KRAS mutant colorectal cancer. Cell Death & Disease, 2021 (PubMed: 34775496) [IF=8.1]

Application: WB    Species: Human    Sample: HCT116 and DLD-1 cells

Fig. 4 Cetuximab activates p38 MAPK and regulates the Nrf2/HO-1 axis. A Western blot analysis of p-p38, total p38, Nrf2 and HO-1 expression levels in HCT116 and DLD-1 cells incubated with cetuximab (100 μg/ml), SB202190 (1 μM) or cetuximab in combination with SB202190 for 24 h. B HCT116 and DLD-1 cells were treated with cetuximab (100 μg/ml) or RSL3 (1 μM) in the absence or presence of SB202190 (1 μM) for 24 h, and cell viability was assessed by the CCK-8 assay. C The protein levels of Nrf2 and HO-1 in HCT116 and DLD-1 cells or Nrf2 overexpressed HCT116 and DLD-1 cells treated with RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. D HCT116 and DLD-1 cells with overexpression Nrf2 were treated with or without RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. Cell viability was assessed by CCK-8 assays. E The protein level of HO-1 in HCT116 and DLD-1 cells or HO-1 overexpressed HCT116 and DLD-1 cells treated with RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. F HCT116 and DLD-1 cells with overexpression HO-1 were treated with or without RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. Cell viability was assessed by CCK-8 assays. G–H HCT116 and DLD-1 cells were treated with cetuximab (100 μg/ml) or RSL3 (1 μM) with or without t-BHQ (20 μM) or hemin (20 μM) for 24 h, and cell viability was assessed by the CCK-8 assay. **P < 0.01.
4). Protective effect of synbiotic combination of Lactobacillus plantarum SC-5 and olive oil extract tyrosol in a murine model of ulcerative colitis. Journal of translational medicine, 2024 (PubMed: 38528541) [IF=7.4]
5). DADLE promotes motor function recovery by inhibiting cytosolic phospholipase A2 mediated lysosomal membrane permeabilization after spinal cord injury. British journal of pharmacology, 2024 (PubMed: 37766498) [IF=6.8]
6). Integrated Multi-Omics Analysis Reveals Mountain-Cultivated Ginseng Ameliorates Cold-Stimulated Steroid-Resistant Asthma by Regulating Interactions among Microbiota, Genes, and Metabolites. International journal of molecular sciences, 2024 (PubMed: 39201796) [IF=5.6]

Application: WB    Species: Mouse    Sample: lung tissues

Figure 9. Integrated analysis of potential mechanisms and validation of PI3K-Akt/MAPK signaling pathway in the combination of DEX and MCG for the treatment of CSRA. (A) Correlation network of DEGs and DEMs. (B) Heatmap of correlation between DEGs and flora. (C) Heatmap of correlation between DEMs and flora. (D) ROC curve analysis. (E) Flora–gene–metabolite–pathway network. (F) Representative western blotting images. (G) Densitometric quantification of protein expression. Reference: GAPDH. (ns, non-significant; * p < 0.05; ** p < 0.01; *** p < 0.001).
7). Candida utilis Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice via NF-κB/MAPK Suppression and Gut Microbiota Modulation. International journal of molecular sciences, 2025 (PubMed: 40076616) [IF=5.6]
8). Protective effect of remdesivir against pulmonary fibrosis in mice. Frontiers in Pharmacology, 2021 (PubMed: 34512328) [IF=5.6]

Application: WB    Species: Mice    Sample: lung tissues

FIGURE 6 Remdesivir inhibits TGF-β1-induced activation of Smad and non-Smad signaling pathway in lung fibroblasts (A) Luciferase assays of CAGA-NIH3T3 cells. Cells were pretreated with Remdesivir (0–50 μM) for 30 min and then incubated with TGF-β1 (5 ng ml−1) for 24 h, then analyzed with luciferase assay. SB431542 is a TGF-β1/Smad pathway inhibitor and serves as a positive control (B) NIH-3T3 cells were co-treated with TGF-β1 (5 ng ml−1) and Remdesivir (12.5, 25, 50 μM) for 1 h. P-Smad3 and Smad3 were assessed using western blot. GAPDH was used as the internal control (C) PPF cells were co-treated with TGF-β1 (5 ng ml−1) and Remdesivir (12.5, 25, 50 μM) for 1 h. P-Smad3 and Smad3 were assessed using western blot. GAPDH was used as the internal control (D) NIH-3T3 cells were co-treated with TGF-β1 (5 ng ml−1) and Remdesivir (12.5, 25, 50 μM) for 1 h and the phosphorylation levels of P-38, JNK, ERK and Akt were analyzed by Western blot. β-tubulin was used as a loading control in grayscale analysis. Scale bar = 60 μm. Data was presented as the means ± SD, n = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
9). The probiotic Lactobacillus plantarum alleviates colitis by modulating gut microflora to activate PPARγ and inhibit MAPKs/NF-κB. European journal of nutrition, 2024 (PubMed: 39607600) [IF=5.0]
10). Qingyihuaji Formula promotes apoptosis and autophagy through inhibition of MAPK/ERK and PI3K/Akt/mTOR signaling pathway on pancreatic cancer in vivo and in vitro. Journal of Ethnopharmacology, 2023 (PubMed: 36690307) [IF=4.8]
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