MAFK Control Peptide
- Known as:
- MAFK Control Peptide
- Catalog number:
- AP13188CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- MAFK Control Peptide
Related genes to: MAFK Control Peptide
- Gene:
- MAFK NIH gene
- Name:
- MAF bZIP transcription factor K
- Previous symbol:
- -
- Synonyms:
- P18, NFE2U
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-24
- Date modifiied:
- 2016-10-05
Related products to: MAFK Control Peptide
Related articles to: MAFK Control Peptide
- Hypoxic injury is a major contributor to cognitive impairment (CI), but the lipid metabolic mechanisms linking hypoxia (HYP) to hippocampal ferroptosis remain understood. This study investigated whether the arachidonate 15-lipoxygenase-cytosolic phospholipase A2 group IVC-lysophosphatidylcholine 18:0 (ALOX15-PLA2G4C-LPC18:0) axis contributes to HYP-induced hippocampal ferroptosis and CI. Morris water maze testing, Nissl staining, and NeuN immunofluorescence showed that HYP impaired spatial learning and memory and induced hippocampal neuronal loss in mice. Semi-targeted LC-MS/MS lipidomics revealed marked phospholipid/lysophospholipid (PL/LPL) remodeling, characterized by increased phosphatidylcholine and phosphatidylethanolamine species and decreased lysophosphatidylcholine species, particularly LPC18:0. Ferroptosis-related biochemical assays and transmission electron microscopy further demonstrated glutathione (GSH) depletion, malondialdehyde (MDA) accumulation, glutathione peroxidase 4 (GPX4) downregulation, and mitochondrial abnormalities. GEO dataset analysis, qRT-PCR, and Western blotting identified ALOX15 as a HYP-responsive ferroptosis-associated regulator. Hippocampal AAV-mediated Alox15 knockdown improved cognitive performance, preserved hippocampal neurons, suppressed lipid peroxidation, and partially restored PL/LPL homeostasis. In HYP-exposed SH-SY5Y cells, genetic and pharmacological experiments further supported the contribution of ALOX15 to ferroptosis-related injury. RNA sequencing, promoter-reporter assays, and gain- and loss-of-function experiments suggested that ALOX15 suppressed PLA2G4C expression partly through MAFK-dependent transcriptional modulation. PLA2G4C restoration increased LPC18:0 production, whereas LPC18:0 supplementation attenuated ferroptosis-related injury and improved hippocampal pathology and cognitive performance in HYP-exposed mice. Collectively, these findings support the ALOX15-PLA2G4C-LPC18:0 axis as a potential lipid-remodeling mechanism underlying HYP-induced hippocampal ferroptosis and highlight ALOX15 inhibition and LPC18:0 restoration as potential strategies for mitigating HYP-induced CI. - Source: PubMed
Publication date: 2026/08/26
Li ZhenGao JieFu JunZhang XiZhou YiyangLi ChenNam JutaekGao Hongchang - Musculoaponeurotic fibrosarcoma oncogene homolog K (MAFK) and amphiregulin (AREG) promote non-small cell lung cancer (NSCLC) progression. However, whether MAFK regulates AREG to mediate the escape of NSCLC cells from doxorubicin (DOX)-induced senescence remains unclear. In the present study, chemotherapy-modulated senescence-related genes were identified through bioinformatics analysis. Human non-small cell lung adenocarcinoma cell lines (A549 and PC-9 cells) were treated with DOX to generate persistent A549 cells (PACs) and persistent PC-9 cells (PPCs). The expression levels of MAFK, AREG and the senescence-associated protein p21 wild-type p53-activated fragment 1 (p21waf1) were evaluated using western blotting and reverse transcription-quantitative PCR. Senescence-associated β-galactosidase staining and colony formation assays were performed to assess cellular senescence and proliferation. The proportions of senescent and proliferating PACs and PPCs were quantified using flow cytometry. A chromatin-immunoprecipitation assay was performed to examine the regulatory association between MAFK and AREG. AREG was associated with cellular senescence, as demonstrated by changes in senescence markers. In A549 and PC-9 cells, DOX treatment upregulated p21waf1 expression, induced senescence, inhibited proliferation and downregulated both MAFK and AREG expression. By contrast, PACs/PPCs exhibited enhanced proliferation alongside elevated MAFK and AREG levels. PACs and PPCs comprised 60-70% senescent cells and 30-40% proliferating cells. MAFK bound directly to the AREG promoter region. In addition, MAFK overexpression reversed the suppressive effect of AREG knockdown on the proliferation of A549 and PC-9 cells. Collectively, MAFK enabled NSCLC cells to escape DOX-induced senescence by upregulating AREG and facilitated cell proliferation upon DOX treatment. - Source: PubMed
Publication date: 2026/05/13
Fan NingningLiang GuanyingShao JiayueWang QiFu Lu - There are few studies on the genomics of heat stress response and the molecular mechanisms of thermoregulation. In this experimental model, Sprague-Dawley rats were subjected to temperatures of 22 ± 1 °C (control group; CT) and 42 °C for varying durations (30, 60, and 120 min, H30, H60, and H120, respectively). Significantly high rectal body temperatures were recorded post-heat stress across all treatment groups. Adrenal corticosterone levels increased significantly, especially in H120 group. Heat stress predictive accuracies of adrenal corticosterone at H60 and H120 were higher with relatively high sensitivity and AUC greater than 0.85. RNA-sequencing of adrenal gland tissue from CT vs. H30, CT vs. H60, and CT vs. H120 identified 4, 8 and 8 known; and 72, 305 and 160 de novo differentially expressed lncRNA (DElncRNAs), respectively. A total of 61, 208, and 124 genes were found to interact with DElncRNAs in the three comparisons, of which 1, 24, and 20 were differentially expressed transcripts (DETs), respectively. Among these known DElncRNAs, Gng 2-202, MAFK-203, Rab32-201, AABR07048992.1-201 were enriched in all three comparisons. Functional enrichment and interaction network analysis of DETs interacting with DElncRNAs indicated their enrichment in pathways related to inflammation-metabolism nexus determined by DETs like Jun, Map3k5, Cyp1b1, Tiparp, Ezh2, and Cbx4. This study will supplement our understanding of the transcriptome level response mechanism of rat adrenal tissue under heat stress and provide theoretical reference for the study of mammalian body response to heat stress stimulation. - Source: PubMed
Publication date: 2026/05/16
Gu JingyiSammad AbdulGuo RenyunKang ShuaiMuniz Maria Malane MagalhãesXu YaxiSheng XihuiDou Jinhuan - Planthoppers, the brown planthopper (BPH, Nilaparvata lugens), white-backed planthopper (WBPH, Sogatella furcifera), and small BPH (SBPH, Laodelphax striatellus) are among the most destructive rice pests in Asia. Neonicotinoid insecticides, particularly imidacloprid, have been widely deployed for their control, but intensive use has driven rapid evolution of high-level resistance across multiple species and regions. Long-term monitoring reveals pronounced spatial and temporal variation in resistance levels, shaped by local selection pressure and seasonal migration dynamics. Resistance is predominantly mediated by metabolic detoxification, with cytochrome P450 monooxygenases (CYPs), especially CYP6ER1 in BPH and its orthologs in WBPH and SBPH playing a central role, as confirmed by RNAi, heterologous expression, and genome-editing studies. Carboxylesterases, glutathione S-transferases, UDP-glycosyltransferases, and ATP-binding cassette transporters contribute additional detoxification capacity, whereas target-site mutations in nicotinic acetylcholine receptors remain comparatively minor in field populations. Transcriptomic analyses reveal that regulatory networks, including CncC/MafK, HNF4, and MAPK signaling-govern CYP overexpression, with comparative evidence highlighting convergent evolution of detoxification pathways across species. This review synthesizes current knowledge on resistance monitoring, molecular mechanisms, and evolutionary dynamics of neonicotinoid resistance in rice planthoppers, with emphasis on the BPH-imidacloprid system and comparative insights from WBPH and SBPH. Implications for integrated resistance management and sustainable pest control, including RNAi-based approaches, are also discussed. - Source: PubMed
Choi MinyoungKhan MurtazaKim Juil - Liver resection is the primary curative treatment for early-stage hepatocellular carcinoma (HCC); however, high recurrence rates remain a major challenge in the absence of effective prognostic and preventive strategies. Here, we identified surgery-induced C-C motif chemokine ligand 11 (CCL11) as a pivotal driver of HCC recurrence through dual mechanisms of immunosuppression and tumor invasiveness. Elevated postoperative circulating CCL11 levels correlated strongly with HCC recurrence and poorer survival, and their integration with clinical parameters enhanced the predictive accuracy of HCC recurrence. Mechanistically, hepatic injury-induced CCL11 recruited immunosuppressive CCR5CD206 M2-like macrophages into the residual liver. These macrophages exhibited enhanced PD-L1 expression via activation of the CCL11/IKK/IκB/NF-κB1 axis and promoted regulatory T cell (Treg) induction from naïve CD4 T cells. Concurrently, CCL11-CCR3 signaling in HCC cells activated PI3K/AKT/MafK to upregulate MMP13, enhancing the invasion ability of HCC cells. In orthotopic models, CCL11 enrichment increased tumor burden and extrahepatic metastases, while post-resection anti-CCL11 therapy reduced HCC recurrence and extended the survival rate of tumor-bearing mice. Our findings unveil CCL11 as a master regulator of the pro-tumorigenic niche post-resection, driving recurrence through coordinated immune evasion and promoting tumor invasiveness. Targeting the CCL11-CCR5/CCR3 axis presents a promising strategy to improve HCC surgical outcomes. - Source: PubMed
Publication date: 2026/02/19
Wang JiaqiYeung Oscar Wai-HoQiu WenqiPang LiLiu JiangYang XinxiangZeng ShinuanDing TaoWang ZheHu ZhenhuaCheung Tan ToMan KwanNg Kevin Tak-Pan