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
- Cuproptosis, a newly discovered form of copper-driven regulated cell death, has been shown to be closely related to ovarian function. However, whether the oocyte dysfunction, decreased ovulation efficiency, and cumulus cell aging caused by copper overload or imbalance are associated with regulatory pathways related to cuproptosis remains unclear. In this study, the expression profiles of genes related to cuproptosis in cumulus cells were comprehensively analyzed through transcriptome sequencing and metabolome analysis, and key genes and pathways that affect oocyte maturation were identified in response to elesclomol and CuSO treatment. Transcriptome analysis of cumulus cells revealed the differential expression of genes involved in key biological processes, such as cellular senescence (AKT3, MORC3, RBL1, etc.), gap junctions (GJA1, GNAI1, GJB3, etc.), steroid biosynthesis (FDX1, HSD17B7, CYP1A1, etc.), and cell cycle regulation (CDK2, CCNB2, MAPK7, etc.). Metabolomic analysis revealed significant changes in the levels of malic acid, PS (18:3(10,12,15)-OH(9)/14:0), and PA (21:0/LTE4), among other compounds. Subsequent Smart-seq analysis of oocytes revealed that after cuproptosis was induced in cumulus cells, oocyte maturation was disrupted, which affected genes associated with cellular senescence (TGFB2, SIRT1, CHEK2, etc.), oocyte meiosis (FBXO5, CCNB3, PLK1, etc.), and DNA methylation (PPM1D, DNMT3B, KMT2A, etc.). These findings provide deeper theoretical support for the key genes and biological processes involved in cumulus cell regulation and oocyte maturation, further clarifying the regulatory mechanisms of cuproptosis in the field of reproduction. - Source: PubMed
Publication date: 2026/05/05
Xu HongTian TianXu DanDu XiaoxueSu RuiLiang JinghongLiu YingZhang YuqingLiu ChangLiang ShuangLi QingyingDing DeliHan YongshengZhai BoLi JidongChen ChengzhenZhang JiabaoJiang HaoYuan Bao - Transcriptional dysregulation in cancer is accompanied by an anabolic transcriptional response driving proliferation and metabolic adaptation. We previously found that oncogenic ETS variant transcription factor 4 (ETV4) overexpression is associated with DNA replication, glycolytic metabolism, tumor progression, and poor prognosis in non-small cell lung cancer (NSCLC). ETV4 is markedly overexpressed in multiple NSCLC datasets, including TCGA-LUAD and TCGA-LUSC. Importantly, ETV4 expression positively correlates with ubiquitin-specific protease 7 (USP7) and mitogen-activated protein kinase 7 (MAPK7) levels. While the E3 ligase constitutive photomorphogenesis protein 1 (COP1) is known to regulate ETV4 ubiquitination and degradation, ETV4 deubiquitination remains unclear. Our study reveals that USP7 deubiquitinates ETV4 and protects it from K11- and K48-linked ubiquitination and proteasomal degradation in NSCLC cells. ETV4 transcriptionally controls the expression of the MAPK pathway key gene MAPK7, which encodes extracellular signal-regulated kinase 5 (ERK5), and participates in the regulation of cell proliferation. Genetic knockdown or pharmacological inhibition of USP7 affects the transcriptional activity of ETV4 on its target gene MAPK7/ERK5. USP7 inhibitor P22077 significantly attenuates ETV4-MAPK7-induced cell proliferation in vitro and tumor growth in vivo. Furthermore, elevated ETV4, USP7, and ERK5 protein expressions are associated with poor prognosis of NSCLC patients. These findings identify that USP7 regulates the deubiquitination, stability, and transcriptional activity of ETV4, contributing to the malignant phenotype of ETV4. Inhibition of USP7 might be a promising target in NSCLC with the dysregulation of ETV4 or hyperactivated MAPK signaling. - Source: PubMed
Publication date: 2026/05/06
Meng XueZhang JiaxiZhang NingHou YuqiLi YimengKang JiaLi RuxinShi YinghuiWang JuanCheng LixinXing Lingxiao - 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