MAPK10 (JNK3), Active Human Recombinant Protein
- Known as:
- MAPK10 (JNK3), Active Human Recombinant Protein
- Catalog number:
- 40092
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biotech support group
- Gene target:
- MAPK10 (JNK3) Active Human Recombinant Protein
Related genes to: MAPK10 (JNK3), Active Human Recombinant Protein
- Gene:
- MAPK10 NIH gene
- Name:
- mitogen-activated protein kinase 10
- Previous symbol:
- PRKM10
- Synonyms:
- JNK3, p493F12, p54bSAPK
- Chromosome:
- 4q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: MAPK10 (JNK3), Active Human Recombinant Protein
Related articles to: MAPK10 (JNK3), Active Human Recombinant Protein
- This study investigates the therapeutic mechanisms of artemisinin (ARS) and its derivatives in atopic dermatitis (AD) using network pharmacology and molecular docking. Molecules and disease targets were screened using public databases, including SwissTargetPrediction, PharmMapper, and Genecards. Core targets were identified, and a protein-protein interaction (PPI) network was constructed using STRING and Cytoscape for topological analysis. Relevant data were obtained from the DAVID database for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Molecular docking of ARS and its derivatives with target genes was performed using AutoDock, with results visualized in Pymol. A functional PPI network was established, and molecular docking demonstrated strong binding activity between ARS derivatives and target protein. Mitogen-Activated Protein Kinase14 (MAPK14) and Mitogen-Activated Protein Kinase10 (MAPK10) was found to be a common target for their treatment of AD. ARS and its derivatives may treat AD by modulating pathways such as Prolactin signaling, cancer pathways, neuroactive ligand-receptor interaction, and IL-17 signaling. ARS and its derivatives have the potential to treat AD. Artemisinin, artesunate, dihydroartemisinin, artemether, artemisinin and artemisinone could potentially treat AD by targeting MAPK14 and MAPK10. - Source: PubMed
Xu WenjingZhu QianyuChen JiaxingHe JunchenYuan AijieCao PengZhang Litao - Genes play an important role in regulating insulin signaling, adipokines, oxidative stress, lipid metabolism, and inflammation in susceptibility and progression of Metabolic dysfunction-associated steatotic liver disease (MASLD). Among various genes, the LepR gene influences insulin sensitivity and controls lipid metabolism, contributing to the development of MASLD. Our previous study reported that a novel congenic mouse (WSB.db) with a LepR mutation exhibited resistance to MASLD. To further evaluate this strain for resistance, we fed this new mouse strain with LepR mutation and B6.db mice, the mouse model of metabolic disease with a high-fat diet as a second hit for 12 weeks and evaluated the pathophysiology, serum biochemistry, Quantitative real-time polymerase chain reaction (qPCR) to determine the expression of specific genes involved in the development of fatty changes in the liver and hepatic transcriptome signatures in liver tissue. In contrast to db/db (B6.db) mice, which exhibited all the pathological hallmarks for MASLD, the LepR mutant congenic strain was still resistant to developing liver steatosis. Transcriptome analysis with KEGG PATHWAY: hsa04932 revealed significant upregulation of AMPKγ3 and MApk10 (JNK3) in WSB.db mice, suggesting that congenic mice with the LepR mutation are resistant to MASLD without the liver pathology to effect. These results propose that the LepR mutation has a different impact on liver pathology depending on genetic background, indicating upregulation of specific genes in the development of MASLD. This study will facilitate the identification of therapeutic targets against MASLD with LepR mutation. - Source: PubMed
Publication date: 2025/05/06
Arindkar Shailendra KumarSingh SurenderKumar Jerald MaheshNagarajan Perumal - Alzheimer's disease (AD) is the most common cause of dementia. Recent studies have revealed incontrovertible roles of astrocytes in the pathology of AD. Considering the conflicting behaviours of astrocytes in AD brain, they have been proposed to have subtypes. In this study, astrocytes from two publicly available single-nuclei transcriptome datasets were integrated to provide in-depth characterization of astrocyte subtypes in AD. Differentially expressed genes within each astrocyte subtype were analyzed by mapping them onto a human protein-protein interaction network to discover subnetworks with biologically relevant genes. Integrating single-nuclei datasets and using network-based analysis approach led to higher sensitivity in capturing AD-related genes compared to traditional approaches. One of the identified subtypes was highly representative of neurotoxic reactive astrocytes in AD. The results show that A1 reactive astrocytes could have an enhancing role for the amyloid beta and neurofibrillary tangle accumulation through MAPK10, MAPT, and TMED10, which were all found to be differentially expressed in this subtype during AD in our analysis. Moreover, single-nuclei ATAC-Seq data from the same tissue was re-analyzed to evaluate astrocyte subtypes at multi-omic level. It was found that astrocyte subtypes underwent epigenetic reprogramming during AD. Potential transcription factors were also identified for the regulation of the genes that exhibited alterations in both promoter accessibility and gene expression in AD. Comparative analysis of single-nuclei RNA-Seq and ATAC-Seq datasets showed that PTN gene, which was reported to be important for AD pathology, is likely regulated by ATF3 transcription factor in subtype-specific manner in astrocytes. - Source: PubMed
Publication date: 2025/04/29
İlgün AtılayÇakır Tunahan - Atherosclerosis (AS) is a leading cause of cardiovascular diseases, characterized by lipid accumulation in arterial walls. The enzyme Ephx2 (soluble epoxide hydrolase, sEH) is implicated in AS development, but its precise mechanisms and therapeutic potential are not fully understood. - Source: PubMed
Publication date: 2025/03/27
Zhang CaiyuzhenDai YuanwenChen YongCao BoAn JinbingPang Wei - Scientific evidence demonstrates that a very low-calorie ketogenic diet (VLCKD) is effective and beneficial in the treatment of obesity, capable of reversing the methylome associated with obesity and has immunomodulatory capacity. This effect is in part promoted by nutritional ketosis and could be involved in counteracting obesity-related cancer. The aim of this study was to evaluate the effect of nutritional ketosis on the methylation of genes related to tumor processes in patients with obesity and in breast cancer cells. Based on methylome data (Infinium MethylationEPIC BeadChip, Illumina) from patients with obesity treated with a VLCKD for weight loss (n = 10; n = 5 women, age = 48.8 ± 9.20 years, BMI = 32.9 ± 1.4 kg/m2), genes belonging to cancer-related pathways were specifically evaluated and further validated in vitro in MDA-MB-231 (triple negative) and MCF7 (RE positive) breast tumor cells pretreated for 72 h with βOHB, the main ketone body, secretome from visceral (VATs) or subcutaneous (SATs) adipose tissue of patients with obesity. The cell tumoral phenotype was evaluated by proliferation assay and expression of cancer-related genes. VLCKD-induced nutritional ketosis promoted changes in the methylation of 18 genes (20 CpGs; 17 hypomethylated, 3 hypermethylated) belonged to cancer-related pathways with MAPK10, CCN1, CTNNA2, LAMC3 and GLI2 being the most representative genes. A similar pattern was observed in the MDA-MB-231 cells treated with β-OHB, without changes in MCF7. These epigenetic changes paralleled the tumoral phenotype modulated by the treatments. Taking together these results highlight the potential role of VLCKD as an adjuvant to anticancer treatment in groups more susceptible to the development of cancer such as patients with obesity, exerting epigenetic regulation through nutritional ketosis and weight loss. - Source: PubMed
Publication date: 2025/03/27
Lorenzo Paula MIzquierdo Andrea GRodriguez-Carnero GemmaCosta-Fraga NicolasDíaz-Lagares AngelPorca Cristinade Luis DanielTejera CristinaDe Paz LauraCueva JuanBellido DiegoCrujeiras Ana B