MAPK3 (phospho-Tyr204) Antibody
- Known as:
- MAPK3 (phosphorilated-Tyr204) Antibody
- Catalog number:
- abx000287
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MAPK3 (phospho-Tyr204) Antibody
Related genes to: MAPK3 (phospho-Tyr204) Antibody
- Gene:
- MAPK3 NIH gene
- Name:
- mitogen-activated protein kinase 3
- Previous symbol:
- PRKM3
- Synonyms:
- ERK1, p44mapk, p44erk1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2015-09-03
Related products to: MAPK3 (phospho-Tyr204) Antibody
Related articles to: MAPK3 (phospho-Tyr204) Antibody
- Baicalein (BA) is a major bioactive flavonoid derived from Georgi. Accumulating evidence has demonstrated that BA exhibits remarkable antitumor activity. However, the mechanisms underlying its effects in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the potential therapeutic mechanisms of BA in CRC through an integrated approach using network pharmacology (NP), molecular docking, molecular dynamics simulations (MDS), and experimental validation. - Source: PubMed
Publication date: 2026/05/15
Wang JiaheHan KunyuChen BingkunGuo YupeiZhao JinyanZhu XiaoqinLin JiumaoChen Yong - Probiotics are beneficial microorganisms that exert several health-promoting effects, while their metabolites, referred to as postbiotics, have recently gained increasing attention for their therapeutic relevance. The present study elucidates the anticancer potential of Bifidobacterium longum MB BBLM15-derived postbiotic metabolites through an integrated experimental and computational approach. Postbiotic metabolites were extracted from Bifidobacterium longum MB BBLM15 using three different solvents (hexane, dichloromethane, ethyl acetate) and subsequently subjected to metabolic profiling. The cytotoxic potential of the three extracts was assessed against cervical cancer cells (HeLa) using a cell viability assay. Hexane-extracted postbiotic metabolites (HX-PM) showed the most potent cytotoxic activity (IC value 263.6 ± 1.32 µg/ml) against HeLa cells, while exhibiting less cytotoxic (IC value 1363 ± 7.4 µg/ml) effect towards the normal kidney epithelial cells (HEK 293), with a selectivity index of HX-PM of 5.8. The anticancer mechanism of HX-PM was further evaluated through a series of cell-based assays, which reveal that HX-PM exhibits anti-proliferative effects, induces G2/M phase cell cycle arrest, triggers apoptosis, suppresses metastasis, and modulates the intracellular redox status in the cervical cancer cells. GC-MS profiling revealed the presence of multiple bioactive metabolites in HX-PM. To further understand the intracellular mode of action, an in-silico framework encompassing network pharmacology and molecular docking was carried out, which identified PTGS2, PPARG, and MAPK3 as the top three hub candidates, with PTGS2 being the probable key molecular target. Additionally, the postbiotic metabolites demonstrated a synergistic interaction with a standard chemotherapeutic drug, cisplatin, as determined by the Chou-Talalay method, highlighting their prospective role in the adjuvant therapy of cervical cancer. Collectively, this study establishes Bifidobacterium longum MB BBLM15-derived postbiotic metabolites as effective anticancer modulators with considerable therapeutic promise. - Source: PubMed
Publication date: 2026/07/11
Mukherjee AdrijaChakraborty DebrajKhamle Arpita RobelSharma Darsh DPatel HemangShah UmangBanerjee AtanuGupta Parth Sarthi SenRai AnkitKaushik GauravPatel MrudukaPatel GayatriSarkar Ruma - Network pharmacology and bioinformatics approaches may provide valuable insights into pharmacological effects by enabling a system-level understanding of how drugs interact with biological networks rather than single targets. The study aimed to elucidate the therapeutic mechanisms of Azadirachta indica leaf extract (AILE) in hepatotoxicity and hepato-injury (HT/HI) through the identification of pathways and molecular targets via network pharmacology. Phytochemical profiling of AILE was performed by Gas Chromatography-Mass Spectrometry (GC-MS). SMILES structures of identified phytochemicals were retrieved from PubChem, and ADMET properties were assessed. Five non-hepatotoxic compounds with high absorption were prioritized. Their potential targets and hepatotoxicity-related genes were predicted using SwissTargetPrediction and GeneCards, followed by drug-target network construction in Cytoscape. Hub genes were identified through protein-protein interaction (PPI) analysis (STRING) and enrichment studies (ShinyGO, KEGG). Gene regulatory networks were built using TRRUST and miRNet 2.0, and molecular docking was performed to evaluate target-protein binding affinities. In the results, ADMET profiling identified five candidate phytochemicals: Butane, 1,1-diethoxy-3-methyl (B), 1,1,3-triethoxybutane (T), Propane, 1,1,3-triethoxy (P), Gamma-Sitosterol (G), and Caryophyllene (C), with favorable absorption. A total of 478 potential compound targets (BTPGC) were predicted, while 1243 HT/HI-related genes were identified, of which 73 overlapped as potential therapeutic targets. PPI analysis generated a network of 73 nodes and 582 edges. GO enrichment revealed involvement in lipid response, oxidative response, programmed cell death, and apoptosis. CytoHubba highlighted six hub genes (TNF, CASP3, ESR1, MAPK3, EGFR, and HSP90AA1). TRRUST identified 15 transcription factors, while miRNet predicted four regulatory miRNAs (miR-155-5p, miR-122-5p, miR-328, and miR-16). This integrative computational network pharmacology analysis provides novel insights into the pathogenesis of liver diseases (HT/HI) and identifies potential therapeutic targets, exploring biomarkers for future experimental validation and clinical translation. - Source: PubMed
Publication date: 2026/07/07
Kumari MrinaliniSrivastava AtulSubhashini Sharma ShaliniSah Shyam BabuSanjeev Kumar - Angiogenesis, a hallmark of cancer, supports tumour growth and metastasis by establishing an abnormal vascular network, and microRNAs (miRNAs) regulate this process post-transcriptionally. Because evidence in canine mammary tumours (CMTs) remains limited, we profiled 24 putative pro- and anti-angiogenic miRNAs by RT-qPCR in benign and malignant CMTs compared with normal mammary glands, and we predicted angiogenesis-related targets using multiMiR followed by Gene Ontology and KEGG pathway enrichment analyses. Intratumoral angiogenesis was quantified as microvascular density (MVD) and endothelial area (EA) on Factor VIII-immunolabeled sections using QuPath. MVD and EA were higher in malignant than in benign CMTs and peaked in grade III carcinomas. Malignant CMTs showed a progressive shift towards a pro-angiogenic miRNA profile, with significant upregulation of pro-angiogenic miR-9, miR-20a, miR-98, miR-210, and miR-21(p < 0.05). Conversely, anti-angiogenic miRNA displayed a heterogenous, context-dependent expression pattern: miR-152-3p and miR-542-3p were downregulated in benign CMTs relative to normal mammary tissue, whereas miR-205 and miR-34a were upregulated in malignant CMTs (p < 0.05). In malignant CMTs, MVD correlated with EA (r = 0.8, p = 0.0003), EA correlated with miR-98 (r = 0.67, p = 0.006), and tumour size correlated with miR-210 (r = 0.58, p = 0.03). In benign tumours, EA correlated with miR-497 (r = 0.81, p = 0.02). Target prediction identified 16,910 genes, with pro- and anti-angiogenic miRNAs sharing 86.5% of predicted targets, indicating extensive regulatory overlap. KEGG enrichment highlighted 100 significantly enriched pathways (FDR < 0.05), including MAPK, PI3K-Akt, HIF-1, VEGF, and breast cancer signalling, with MAPK1 and MAPK3 among the most frequently targeted genes. Finally, miR-34a showed the best diagnostic performance for distinguishing benign from malignant CMTs. Overall, findings support a substantial contribution of miRNAs to angiogenic regulation in CMTs, strengthen the utility of the canine model in comparative breast cancer research, and highlight the potential of miRNA-based biomarkers for tumour stratification and anti-angiogenic targeting. - Source: PubMed
Publication date: 2026/07/04
Abbate Jessica MariaGiosa DomenicoAnjomanibenisi MaralArfuso FrancescaGiannetto AlessiaCapra Anna PaolaRiolo KristianLanteri GiovanniBrunetti Barbara - ObjectiveVisceral adipose tissue (VAT) produces several adipokines; however, VAT adipocytes' gene expression has not been related with cardio-metabolic components. The present study aimed to explore associations between gene expression in human primary VAT adipocytes' and cardio-metabolic components in subjects who live with Metabolically Unhealthy Obesity (MUO) compared with subjects who live with Metabolically Healthy Obesity (MHO).MethodsCross-sectional study of patients who live with obesity, who underwent bariatric/metabolic surgery.ResultsForty-five patients (18 MHO and 27 MUO) aged 44 years, main co-morbidities Diabetes and Hypertension, were analyzed. MUO showed younger age and higher cardio-metabolic risk, as well as larger adipocyte´s sizes. Primary cultured adipocytes were isolated from trans-surgical VAT sample, then cDNA was analyzed for the expression of 92 genes, further distributed as MUO MHO and clustered according to their linkage with cardio-metabolic components. Higher expression of genes like EDN1, IL-6, ADIPOQ, GSTA2, TGFβ, WNT3A, KDR, MAPK3, vWF (p<0.04); as well as reduced NOS2, PDGFA, HAMP and RARRES2 (p<0.01) were observed across clusters of hyperglycemia, hypertension, dyslipidaemia, and central obesity, broadly implicating pathways related to inflammation, oxidative stress, endothelial dysfunction, insulin resistance, and vascular regulation.ConclusionFindings from the present exploratory analysis show that cardio-metabolic risk is associated to VAT adipocytes' gene expression; particularly those genes related to oxidative stress, insulin resistance, inflammation, endothelial dysfunction, athero-thrombosis, and lower vasodilation. Further longitudinal and mechanistic studies are required to clarify the directionality and clinical significance of these associations. - Source: PubMed
Publication date: 2026/07/04
Suárez-Cuenca Juan AntonioHernández-Patricio AlejandroVera-Gómez EduardoGutiérrez-Buendía Juan ArielRuíz-Hernández Atzín Suáde la Vega-Moreno KarenDe la Peña-Sosa GustavoMontoya-Ramírez JesúsMelchor-López AlbertoDiaz-Aranda María AngélicaBernal-Figueroa YareniMartínez-Torres Gustavo IvánGutiérrez-Salinas JoséAlcaráz-Estrada Sofía LizethGarcía SilviaPineda-Juárez Juan AntonioToledo-Lozano Christian GabrielRamos-Vázquez Dulce CeciliaDelaflor-Wagner Christian AlejandroTéllez-González Mario AntonioMondragón-Terán PaulZermeño-Ugalde Pablo