Ask about this productRelated genes to: MAFK Blocking 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 Blocking Peptide
Related articles to: MAFK Blocking Peptide
- 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 - Triple-negative breast cancer (TNBC) remains a major clinical challenge, owing to its molecular complexity, therapeutic resistance, and lack of specific druggable targets. The herpes simplex virus thymidine kinase/ganciclovir (HSV-TK/GCV) suicide gene therapy system has shown promise in cancer treatment, but its clinical applicability is limited by off-target cytotoxicity. Here, we developed a breast cancer-specific suicide gene circuit (BRAS) that integrates the screened cancer-specific promoters RRM2 and MAFK with a microRNA specific to nontumor cells, utilizing the distinct molecular profiles of tumor and nontumor cells. This multi-input logic gate circuit enables precise, specific expression of HSV-TK in breast cancer cells with hardly expression in normal cell. We show that BRAS selectively induces apoptosis in patient-derived TNBC cells while sparing normal cells. In two orthotopic breast cancer models, BRAS significantly suppressed tumor growth without affecting body weight or general health, underscoring its therapeutic potential. This approach intelligently combines molecular signals from both cancerous and healthy cells to precisely regulate therapeutic gene expression, making it a promising platform for the next-generation cancer therapy. - Source: PubMed
Publication date: 2026/02/04
Tang ShashaFang YuanJin LingliLiu DongyangLiu YichengZheng RuijiaYong LiyunWu XinQiao LongliangWang MeiyanCai Fengfeng - Transposable elements (TEs) occupy nearly half of the human genome and play diverse biological roles. Despite their abundance, the extent to which TEs contribute to three-dimensional (3D) genome structure remains unclear. - Source: PubMed
Publication date: 2026/01/20
Shi LiyangXiao ZhenZhou XuemengBabarinde Isaac AFu XiulingMa GangHuang ZhuoqiSun LiHe JiangpingStrunnikov AlexanderHutchins Andrew P - Lambda-cyhalothrin (λ-cyhalothrin) is a broad-spectrum pyrethroid against lepidopteran pests, yet its efficacy is increasingly threatened by insect resistance. Although overexpression has been implicated in λ-cyhalothrin detoxification in , the regulatory mechanism remains unclear. Here, CRISPR/Cas9-generated knockout increased larval susceptibility to λ-cyhalothrin, confirming its essential role in detoxification. λ-Cyhalothrin exposure triggered the expression of several transcription factors, including , , , , , and . Their knockdown suppressed expression, thereby compromising larval tolerance. Dual-luciferase reporter assay demonstrated that these transcription factors regulated transcription by binding to the specific -acting elements. Moreover, protein kinases AKT, ERK, JNK, and RSK2 were implicated as upstream regulators, orchestrating transcription factor expression and subsequent CYP6AE48-mediated detoxification. These findings reveal a multilayered regulatory circuitry that activates expression to facilitate λ-cyhalothrin detoxification, providing novel insights into the evolutionary adaptation of detoxification mechanisms and highlighting potential molecular targets for future pest management strategies. - Source: PubMed
Publication date: 2026/01/04
Ma WenlingYang ZhimingLu Kai - This study aimed to explore the mechanism by which salidroside alleviates lung ischemia-reperfusion injury (LIRI) through the lncRNA PTOV1-AS2/miR-525-5p/ACE2 axis, with a specific focus on its role in regulating ferroptosis. In the murine model of LIRI, we administered salidroside either alone or in combination with adenoviral vectors for overexpression or knockdown of PTOV1-AS2 or ACE2. Subsequently, we examined lung histopathological changes, evaluated the severity of pulmonary edema, and assessed the levels of lung damage and inflammation. Additionally, an in vitro model was established using MLE12 cells induced by oxygen-glucose deprivation/reoxygenation (OGD/R), and relative cell viability and reactive oxygen species (ROS) levels were measured. The interactions between PTOV1-AS2 and miR-525-5p, as well as between miR-525-5p and ACE2, were predicted and confirmed through a series of assays. Moreover, the relationship between the transcription factor MAFK and lncRNA PTOV1-AS2 was investigated. The results revealed that salidroside upregulated ACE2 expression, thereby reducing lung injury, inflammation, and ferroptosis in both LIRI mice and OGD/R-induced MLE12 cells. Mechanistically, PTOV1-AS2 served as a competing endogenous RNA (ceRNA) to sponge miR-525-5p, thereby enhancing ACE2 expression, and this regulatory effect was further strengthened by salidroside treatment. Furthermore, it was found that MAFK directly bound to the promoter of PTOV1-AS2, promoting its transcription and subsequent expression. In conclusion, salidroside enhances resistance to ferroptosis and alleviates LIRI through the MAFK/PTOV1-AS2/miR-525-5p/ACE2 signaling axis, which provides new insights into the therapeutic potential of salidroside in LIRI. - Source: PubMed
Yu XiaoboXu BinbinZhang MingdongYao XuelianXu KunXie XiaoxiaoShen XiaoGao Fengying