Ask about this productRelated genes to: MAPK7 antibody
- Gene:
- MAPK7 NIH gene
- Name:
- mitogen-activated protein kinase 7
- Previous symbol:
- PRKM7
- Synonyms:
- BMK1, ERK5
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2014-11-19
Related products to: MAPK7 antibody
Related articles to: MAPK7 antibody
- Polycystic ovary syndrome (PCOS) involves oxidative stress-driven ovarian dysfunction and remains difficult to treat due to drug side effects and poor target engagement. We engineered a reactive oxygen species (ROS)-responsive, macrophage-membrane-camouflaged quercetin nano-therapy (MM@PCD@QNPs) to enhance ovarian delivery and mitigate toxicity. The core comprises a pinacol phenylboronate-dextran conjugate that encapsulates quercetin and undergoes ROS-triggered release; a surface M0 macrophage membrane confers immune evasion and lesion tropism via retained proteins (e.g., CD11b and CD47-SIRPα). MM@PCD@QNPs displayed nanoscale dimensions and stability (133.63 ± 14.60 nm; -33.13 ± 1.52 mV) and released drug under elevated ROS. In DHT-injured granulosa cells and a DHEA-induced PCOS mouse model, the formulation promoted granulosa cell proliferation, suppressed apoptosis, reduced ROS, and preferentially accumulated in ovaries, with negligible in vitro and in vivo toxicity. Transcriptomics and validation implicate activation of the MAPK7-Nrf2-NQO1 axis as a principal mechanism; pharmacologic MAPK7 inhibition abrogated therapeutic effects. By coupling ROS-triggered release with macrophage-mimetic targeting, MM@PCD@QNPs overcome quercetin's low bioavailability and off-target exposure and provide a safe, effective nanoplatform for PCOS therapy. - Source: PubMed
Publication date: 2026/02/21
Li WenzhuGuan YuSong NanZhang FengDeng ZhiminYin TailangYang YanbingConde JoãoJin WenyiYin Zhinang - Inflammatory bowel disease (IBD) and rheumatoid arthritis (RA) are chronic inflammatory diseases that share immune dysregulation and mitochondrial dysfunction. Understanding the molecular mechanisms linking these diseases to mitochondrial dysfunction is crucial for developing novel diagnostic and therapeutic strategies. Datasets related to IBD and RA were obtained from the Gene Expression Omnibus database. Differentially expressed mitochondrial dysfunction-related genes (MDRGs) were identified using differential expression analysis. Weighted gene co-expression network analysis was performed to identify crosstalk genes (CGs). Logistic regression and support vector machine (SVM) models were constructed using least absolute shrinkage and selection operator regression to identify hub genes. Additionally, the differential expression and diagnostic value of the hub genes were verified using quantitative reverse transcriptase-polymerase chain reaction and validation sets. Finally, immune infiltration analysis was conducted to assess the role of immune cells in IBD and RA. A total of 87 CGs associated with mitochondrial dysfunction were identified between IBD and RA, among which and were identified as hub genes. Twenty proteins, including ERO1A, MAPK7, and P4HB, were identified as key proteins that interacted with PDIA4 and DUSP6. The area under the curve (AUC) of the ROC curves for IBD and RA based on the and diagnostic models were 0.664 and 0.856, respectively. The qRT-PCR results indicated that and were overexpressed in IBD and RA. Seven immune cell types, including activated B cells, activated dendritic cells, and eosinophils showed significant differences in the IBD and RA groups. Our findings highlight the close association between IBD, RA, and mitochondrial dysfunction. and may serve as potential biomarkers of mitochondrial dysfunction in patients with IBD and RA. - Source: PubMed
Publication date: 2026/01/16
Cui LijiaoYe ShicaiGu ZhiweiZhang GuixiaChen TingenZhou YuYu Caiyuan - The extracellular signal-regulated kinase 5 (ERK5) signaling pathway represents a promising therapeutic target for non-small cell lung cancer (NSCLC), yet the development of potent and selective inhibitors remains a challenge. Leveraging the 5,7-diazaindole scaffold, a privileged structure in kinase inhibitor discovery, we designed, synthesized, and evaluated a novel series of derivatives as potential ERK5 inhibitors. Among them, compound I1 emerged as the most potent candidate, demonstrating significant anti-proliferative activity against A549 human lung cancer cells with an IC₅₀ of 40.1 μM. Critically, an in vitro kinase assay confirmed that I1 is a direct ERK5 inhibitor, exhibiting potent inhibition of purified ERK5 kinase activity with an IC₅₀ of 403.4 nM. Structure-activity relationship (SAR) studies underscored the critical importance of the unsaturated 1,2,3,6-tetrahydropyridine ring, the amide carbonyl group, and the N1H moiety for optimal activity. Molecular docking revealed that I1 binds robustly within the ERK5 ATP-binding site (PDB: 6HKM), forming key hydrogen bonds with Met140, Asp138, and Asp200, and exhibiting a more favorable binding mode than its analogues. Mechanistic studies indicated that I1 functions as a direct ERK5 inhibitor, suppressing both ERK5 phosphorylation and total protein expression. This ERK5 inhibition triggered a multi-modal anti-tumor mechanism, including the induction of endoplasmic reticulum stress, mitochondrial dysfunction (characterized by reactive oxygen species accumulation and loss of membrane potential), and ultimately, activation of the mitochondrial apoptotic pathway. Importantly, I1 exhibited significant dose-dependent tumor growth suppression in a Lewis lung carcinoma mouse model without causing observable toxicity, highlighting its potential as a promising lead compound for targeted NSCLC therapy. - Source: PubMed
Publication date: 2026/01/16
Tian BinbinLi YunjieXue PengyuChen RenhaoLv ShuoHe LuqianLin GaoyangXiao JunLong LinCao GuoruiGuo ChuanlongHuang Longjiang - Cancer remains a major global health challenge and is the second leading cause of mortality worldwide. Despite extensive efforts, the development of effective cancer therapies is still limited. Mitogen-activated protein kinase 7 (MAPK7), a critical regulator of cell proliferation, gene transcription, and metabolism, has recently emerged as a promising therapeutic target for cancer intervention. In this study, we applied advanced machine learning-based computational approaches to identify potential MAPK7 inhibitors. Virtual screening of a large library of drug-like molecules using machine learning models identified 33 active compounds against MAPK7. Molecular docking further refined these hits to five compounds with favorable binding affinities and strong interactions with key catalytic residues. Molecular dynamics (MD) simulations provided additional insights into the stability and conformational dynamics of protein-ligand complexes, highlighting amino acid residues crucial for inhibitor retention within the active site. Collectively, our findings suggest that these five compounds represent promising MAPK7 inhibitors, offering new opportunities for the development of targeted cancer therapeutics. To the best of our knowledge, this is the first study to combine machine learning-based virtual screening, molecular docking, and MD simulations for the identification of MAPK7 inhibitors. - Source: PubMed
Publication date: 2026/01/08
Hayat ChandniAjmal AmarGul NayabNuman MuhammadBibi HaleemaAkhtar NaveedSultan LaibaAli ArifKhan Muhammad TahirSaqib Muhammad - Mitogen-activated protein kinases (MAPKs) are a family of evolutionarily conserved serine/threonine protein kinases that can be activated by diverse stimuli. They transmit signals from the cell membrane to the nucleus, regulating various biological processes such as apoptosis, hormone signaling, and immune responses. Members of the MAPK family have been extensively studied in multiple species and have been confirmed as a central hub for regulating antibacterial immunity and hypoxia adaptation in perciform fishes, such as Asian seabass and groupers. Given that the large yellow croaker, as an important mariculture species within this order, faces serious threats from Pseudomonas plecoglossicida infection and hypoxic stress, deciphering the functions of its MAPK family is of significant importance. To this end, this study identified 16 mapk genes in the large yellow croaker. Phylogenetic analysis revealed that these mapk genes were classified into three major subfamilies: ERK, JNK, and p38 MAPK. Comparative analyses of gene structures and conserved protein motifs demonstrated high conservation among MAPK family members. Meanwhile, RNA-seq data following bacterial and hypoxic stress revealed distinct expression patterns of mapk genes. mapk7, mapk10, and mapk14a exhibited significant differential expression in response to P. plecoglossicida challenge, and mapk7, mapk8b, and mapk14a were significantly induced under hypoxia stress, implying their potential involvement in stress adaptation. The protein-protein interaction (PPI) network analysis revealed that MAPK family members (including MAPK3, MAPK7, MAPK8b, MAPK12a, MAPK13, and MAPK14a) in Larimichthys crocea exhibit close interactions with key signaling proteins (such as MAP2K1, c-Fos, AP-1, and MAPKAPK2). These interactions suggested the potential formation of a complex signal transduction network involved in the immune stress response, collectively mediating the immune stress regulation in Larimichthys crocea. These findings enhanced the understanding of environmental adaptation mechanisms in large yellow croaker, and provided crucial candidate target genes and a theoretical basis for in-depth analysis of its molecular responses to pathogen infection and hypoxic stress. - Source: PubMed
Publication date: 2025/12/17
Wang ZiyuHan PingXue YadongChen JianmingLiu XiumeiWang Xubo