Ask about this productRelated genes to: PFKFB4 antibody
- Gene:
- PFKFB4 NIH gene
- Name:
- 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-04
- Date modifiied:
- 2016-10-05
Related products to: PFKFB4 antibody
Related articles to: PFKFB4 antibody
- - Source: PubMed
Publication date: 2026/04/15
Gan ChaoWu DanYuan YueLi LinglingBai JiaXu YanmeiLv Haihong - Epstein-Barr virus (EBV) is associated with 200,000 cancers per year, including Burkitt lymphoma and post-transplant lymphomas. We previously reported that EBV latency oncogene programs dynamically remodel infected B cell metabolism and sensitivity to induction of ferroptosis, a programmed cell death pathway driven by lipid reactive oxygen species. However, much has remained unknown about how EBV remodels key redox defense pathways in support of infected B cell proliferation. Here, we identify EBV latent membrane protein 1 (LMP1), a key viral oncogene necessary for B cell immortalization and which mimics aspects of CD40 signaling, drives resistance to ferroptosis induction by erastin, a small molecule that blocks cystine uptake. LMP1 expression was sufficient to protect Burkitt cells from erastin ferroptosis induction. Mechanistically, signaling from the LMP1 TES2/CTAR2 region drove this phenotype, which was not shared by CD40 signaling, revealing that LMP1 evolved independent redox defense roles. Metabolomic analysis highlighted key LMP1 and TES2 signaling roles in support of antioxidant cysteine and glutathione levels. TES2 signaling supported cystine uptake, glutathione and NADPH pools in newly infected peripheral blood B cells. We identified PFKFB4, a host enzyme that shunts glucose into the pentose phosphate pathway to support NADPH production, as a major TES2 metabolic target. PFKFB4 knockdown increased EBV-transformed lymphoblastoid cell line lipid ROS levels, decreased glutathione and strongly sensitized them to ferroptosis induction by erastin treatment. PFKFB4 was also necessary for LMP1-mediated Burkitt B cell ferroptosis resistance. Collectively, these results identify PFKFB4 as a key host cell EBV metabolism remodeling target critical for infected B cell redox defense. - Source: PubMed
Publication date: 2026/03/10
Burton Eric MMitra BidishaGuo RuiAsara John MGewurz Benjamin E - The role of the crosstalk between glycolysis and M2 macrophages in hepatocellular carcinoma (HCC) progression remains incompletely understood. This study aimed to identify prognostic genes linked to both glycolysis and M2 macrophages in HCC and to elucidate their mechanistic underpinnings. - Source: PubMed
Publication date: 2026/02/12
Wang AnqiYou LinaZuo MingHe ZhanaoYang HongHuang Wukui - In this study, we identified a number of biological processes, pathways, and key protein targets associated with coenzyme metabolism in bovine clinical mastitis (CM). The expression patterns and subcellular localization of key proteins were examined to characterize their potential association with oxidative stress and inflammatory responses in mammary gland tissues. The CM group exhibited collapsed and atrophied mammary acini, inflammatory cell infiltration, increased reactive oxygen species fluorescence signals, and a significant reduction in glutathione content. Levels of key coenzymes, including nicotinamide adenine dinucleotide and flavin adenine dinucleotide, decreased significantly. Bioinformatic analysis identified four biological processes related to coenzyme metabolism and 20 key differentially expressed proteins associated with the glycolysis pathway. Among them, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) and PFKFB4 were identified as key hub proteins involved in fructose and mannose metabolism and AMP-activated protein kinase (AMPK) signaling pathways. PFKFB3 and PFKFB4 were primarily localized in the cytoplasm of mammary epithelial cells, and the CM group showed significantly upregulated and downregulated expression at both the gene and protein levels. Molecular mechanism analysis based on pathway enrichment suggested a putative regulatory network in which pathogen-induced inflammation may be associated with ROS-AMPK-related signaling, potentially contributing to dysregulated PFKFB3/PFKFB4 expression, glycolytic imbalance, impaired coenzyme metabolism, and mammary epithelial cell injury. - Source: PubMed
Publication date: 2026/02/12
Yu XingZhang BohaoGao YumengYang ZhenDong WeitaoZhang YongZhao XingxuZhang Quanwei - Bladder cancer (BLCA) is a prevalent genitourinary malignancy characterized by high recurrence and mortality rates. While mannose metabolism has demonstrated anti-tumor potential across various cancers, its role in BLCA remains underexplored. This study examines the influence of mannose metabolism on BLCA prognosis. - Source: PubMed
Publication date: 2026/01/28
Li AnhongZhao KaileWang TianjiaoShi Guangyue