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MAPK2 unactive, <I>E.coli<_I> product offer - Gentaur Molecular Products

MAPK2 unactive, E.coli<_I>


Price:
638.33 €
Known as:
MAPK2 unactive, E.coli<_I>
Catalog number:
Z02687
Product Quantity:
20ug
Category:
-
Supplier:
Genscript
Gene target:
MAPK2 unactive <>.coli<_I>
Ask about this product

Related genes to: MAPK2 unactive, E.coli<_I>

Gene:
MAPK1 NIH gene
Name:
mitogen-activated protein kinase 1
Previous symbol:
PRKM2, PRKM1
Synonyms:
ERK, ERK2, p41mapk, MAPK2
Chromosome:
22q11.22
Locus Type:
gene with protein product
Date approved:
1993-11-05
Date modifiied:
2019-04-23

Related products to: MAPK2 unactive, E.coli<_I>

Related articles to: MAPK2 unactive, E.coli<_I>

  • Multi-dimensional profiling of primary metabolites in Heuchera micrantha varieties reveals potential for functional food development.

    Heuchera micrantha is a horticultural plant with emerging pharmacological value, yet its primary metabolites remain underexplored. This study comprehensively profiled nutrient metabolites in four H. micrantha varieties using LC-MS/MS. We identified 285 metabolites, with amino acid derivatives being predominant. Multivariate analysis revealed distinct varietal accumulation patterns and 204 differential accumulated metabolites (DAMs). Integrative network pharmacology and molecular docking suggested γ-glutamyltyrosine and L-prolyl-L-phenylalanine as potential bioactive dipeptides that may interact with core hubs (MAPK1, EGFR, SRC) involved in cancer and inflammation pathways, though these predictions require experimental validation. Transcriptomics identified 39 differentially expressed genes regulating the biosynthesis of their precursor amino acids. Antioxidant assays showed varietal differences: some excelled in free radical scavenging (DPPH/ABTS) while others demonstrated superior reducing power (FRAP). This multi-omics study suggests that H. micrantha may be a rich source of therapeutically relevant primary metabolites, providing a preliminary scientific basis for its development as a functional food or nutraceutical pending further validation. - Source: PubMed
    Publication date: 2026/07/09
    Meng JinmingWu NaFu HongboGong WeichangXiong Lina
  • New insights into 6PPD-quinone-induced neurotoxicity in zebrafish: the role of the MAPK/oxidative stress axis in neurodevelopmental disruption.

    6PPD-Quinone (6PPD-Q) has attracted widespread attention because of its high toxicity to aquatic organisms. Recent evidence suggests that the acute mortality induced by 6PPD-Q is closely associated with neurotoxicity; however, the key events and underlying molecular mechanisms remain unclear. In the present study, we investigated the effects of 6PPD-Q on neurodevelopment in zebrafish and explored the potential mechanisms involved. Environmentally relevant concentrations of 6PPD-Q did not cause acute lethality, but significantly induced locomotor abnormalities and impaired neuronal development. In parallel, the expression profiles of genes related to neuronal development and neurotransmission were markedly altered. In addition, 6PPD-Q disrupted redox homeostasis, as evidenced by increased ROS and MDA levels and decreased activities of the antioxidant enzymes CAT and SOD. Gene Ontology analysis indicated that the neurotoxic effects of 6PPD-Q were associated with biological processes including positive regulation of the MAPK cascade, cellular response to dopamine, and synaptic signaling. KEGG enrichment analysis further suggested the involvement of the MAPK signaling pathway. Molecular docking showed favorable binding potentials between 6PPD-Q and several MAPK-related targets (binding affinities: -5.16 to -6.25 kcal/mol), while qRT-PCR analysis revealed significant upregulation of MAPK-related genes, including mapk8b, mapk14a, mapkapk2a, map2k1, and mapk1. Furthermore, Western blot analysis demonstrated significantly increased phosphorylation levels of p38, JNK, and ERK following 6PPD-Q exposure, indicating activation of the MAPK signaling pathway. Notably, doramapimod, a selective MAPK inhibitor, partially ameliorated 6PPD-Q-induced defects in neuronal development, abnormal gene expression, and oxidative stress. Collectively, these findings suggest that MAPK-associated oxidative stress contributes to 6PPD-Q-induced neurodevelopmental toxicity in zebrafish. - Source: PubMed
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  • Systematic investigation of a Fraxinus mandshurica seed-derived iridoid glucoside fraction as a novel functional ingredient with anti-diabetic potential.

    Fraxinus mandshurica (Oleaceae, Fraxinus) seeds serve as food and condiments in traditional American and European diets. This study provides the first systematic evaluation of the therapeutic effects of F. mandshurica seed extract on T2DM. This study evaluated the effects of F. mandshurica seed extract on glucose-lipid metabolism, hepatorenal function, and gut microbiota in an HFD/STZ-induced T2DM mouse model. Through UPLC-Q-TOF-MS chemical characterization and phytochemical analysis, combined with network pharmacology and molecular docking techniques, potential active components and their corresponding targets were predicted. Critically, the predicted activity of 18 iridoid monomers was confirmed by evaluating their ability to enhance glucose consumption in L02 cells. F. mandshurica seed extract significantly reduced body weight, TC, TG, and blood glucose levels, improved insulin sensitivity and glucose tolerance, and alleviated hepatorenal injury. Additionally, it regulated the gut microbiota by reducing the Firmicutes/Bacteroidetes ratio. Network pharmacology analysis identified AGE-RAGE and TNF signaling as core anti-diabetic pathways. Key active components, including bisandrographolide A, ligstroside, reptoside, oleuropein, fraxoside, koaburside, and mudanpioside D, were identified and selected for molecular docking. The results indicate that these active components form stable ligand-receptor complexes with target proteins (HRAS, MAPK1, HSP90AA1, MMP9 and AKT1) via hydrogen bonds, hydrophobic interactions, π-π stacking and salt bridges. Finally, 18 iridoid glucosides from the F. mandshurica seed were shown to promote glucose consumption, with efficacy ranging from 7.27% to 71.52%. This study reveals that F. mandshurica seeds and their characteristic iridoid components possess promising prospects as candidates for developing natural anti-diabetic therapeutics. - Source: PubMed
    Publication date: 2026/07/08
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  • Naringenin attenuates amiodarone-induced pulmonary fibrosis in rats via modulation of the SIRT1/NF-κB signalling pathway.

    Amiodarone (AMD)-induced pulmonary fibrosis (PF) is a serious adverse effect driven by oxidative stress and inflammation. Naringenin [NAR], a citrus flavonoid, possesses potent antioxidant and anti-inflammatory properties. This study investigated the protective effects of NAR against AMD-induced PF in rats, focusing on the sirtuin 1; nuclear factor Kappa -B (SIRT1/NF-κB) pathway. - Source: PubMed
    Publication date: 2026/07/08
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    Osteoporosis, a prevalent age-related disease, is characterized by impaired bone formation and an increased risk of fractures. Current anabolic treatments primarily rely on biologics, which are costly and require inconvenient administration. Identifying regulators of osteoblastogenesis that are amenable to small-molecule targeting is essential for developing more accessible therapies. Through an unbiased kinome-wide RNAi screen in primary murine calvarial osteoblasts, we identified the AXL receptor tyrosine kinase (Axl) as a negative regulator of osteoblast differentiation. Axl is most highly expressed in undifferentiated and early differentiated osteoblasts, with a rapid decline in expression during osteoblast maturation. siRNA-mediated knockdown of Axl or pharmacological inhibition with the small molecule BGB324 significantly enhanced osteoblast differentiation and mineralization in vitro. In mice, BGB324 treatment significantly increased bone mass by promoting bone formation. Mechanistically, Axl knockdown or inhibition upregulated interferon-stimulated gene 15 (Isg15), while Isg15 knockdown impaired osteoblast differentiation and enhanced Erk phosphorylation, leading to increased expression of osteoblast-specific genes. Consistently, double knockdown experiments demonstrated that simultaneous loss of Axl with either Isg15 or Mapk1, but not other interferon-related genes, reversed the Axl knockdown-induced increase in osteoblast differentiation, reinforcing their mechanistic involvement. Collectively, our study identifies Axl as a promising therapeutic target for osteoporosis and other bone-related disorders. - Source: PubMed
    Publication date: 2026/07/06
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