Ask about this productRelated genes to: PFKM antibody
- Gene:
- PFKM NIH gene
- Name:
- phosphofructokinase, muscle
- Previous symbol:
- PFKX
- Synonyms:
- PFK-1, PPP1R122
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: PFKM antibody
Related articles to: PFKM antibody
- Lung adenocarcinoma (LUAD), the most widely existing subtype of non-small cell lung cancer (NSCLC), is a leading cause of cancer-related mortality, characterized by challenging early diagnosis, high rates of recurrence and metastasis, and poor prognosis. Chemotherapy remains the primary treatment for advanced LUAD, but its effectiveness is often hindered by the development of chemoresistance. In this study, a targeted metabolomics method unveiled a marked up-regulation of glycolysis in chemotherapy-resistant LUAD cells. Particularly, the ratio of fructose 1,6-bisphosphate (FBP) to fructose 6-phosphate (F6P) reflected the activity of the rate-limiting enzyme phosphofructokinase muscle isoform (PFKM) was significantly elevated. We further observed a significant increase in exosome release in chemotherapy-resistant cells. More importantly, it was found that the interaction between PFKM and exosomes plays a role in regulating chemoresistance in LUAD. Mechanistically, PFKM influences exosomes release by modulating Ras-related protein Rab-8B (RAB8B) expression, impacting apoptosis and glycolytic metabolism, thereby promoting chemoresistance. Furthermore, drug-resistant cells enhance chemoresistance in sensitive cells by releasing exosomes with heightened glycolytic activity. These findings highlight the crucial role of the PFKM-RAB8B axis in promoting chemoresistance, suggesting it as a potential therapeutic target for countering LUAD chemoresistance. - Source: PubMed
Publication date: 2025/09/12
Wang QiangNong QiyaoZang JunguoGao MeiyuZhang YingHao XinyuanTian YuanXu FengguoZhang Pei - Alzheimer's disease (AD) is characterized by progressive neurodegeneration and impaired glucose metabolism. While most studies focus on heavily affected brain regions such as the hippocampus and prefrontal cortex, the visual cortex remains relatively preserved in early AD and provides an opportunity to examine metabolic alterations that precede widespread pathology. - Source: PubMed
Publication date: 2026/04/09
Mjaaseth Ulrik NHsu Ming-FoArballo JosephHaj Fawaz GPatel Viharkumar - The insidious onset and progression of sarcopenia make it vital to understand the early skeletal muscle changes and explore therapies to slow its progression. This study explored the remodeling at an early stage of aging (14 months of age) and the effects of lifelong aerobic exercise. For that, 2-month-old male Wistar rats underwent a 12-month treadmill exercise program. Sedentary age-matched, young sedentary, and young exercised for 6 months rats were considered. The results highlighted an age-related decrease in the relative muscle mass, suggestive of loss or atrophy of some fibers, which was mitigated by lifelong aerobic exercise. Consequently, an age-related compensatory hypertrophy was suggested to be triggered in the muscle. Data proposed that aging reduced mitochondrial density, indicated by citrate synthase (CS) activity, which was prevented by lifelong aerobic exercise. The reduced CS activity correlated with increased ATP-dependent 6-phosphofructokinase (PFKM)/ATP synthase subunit beta (ATPB) ratio, suggesting that at an early stage of aging, the skeletal muscle favors the glycolytic metabolism in response to decreased mitochondrial content. The results also pointed to an age-induced AMP-activated protein kinase (AMPK) activation and an AMPK-related apoptosis inhibition, perchance to reduce fiber loss or atrophy. The basal phosphorylated AMPK/AMPK ratio decreased with lifelong aerobic exercise, possibly reflecting the exercise-induced increase in CS activity. This work highlights the importance of studying early skeletal muscle changes in aging for timely disease management and prevention. - Source: PubMed
Publication date: 2026/04/18
Moreira-Pais AlexandraFerreira RitaNeuparth Maria JoãoFardilha MargaridaMoreira-Gonçalves DanielOliveira Paula ADuarte José A - To characterize the transcriptional and physiological alterations induced by manganese stress in , juveniles (mean weight 5.0 ± 0.2 g) were subjected to either manganese exposure (5.50 ± 0.03 mg/L) or control (0 mg/L) for a 12 h period. Subsequently, gill tissues were excised for evaluation of antioxidant parameters and RNA-Seq analysis. A total of 753 DEGs were identified in the manganese exposure group compared to controls, comprising 287 up-regulated and 466 down-regulated genes. GO and KEGG enrichment analysis of DEGs showed that most of the DEGs were involved in immune and metabolic pathways, which disturbed the biological processes related to immunity and metabolism at the molecular level. The acute manganese stress initiated a multi-level antioxidant response to cope with oxidative stress in . This finding was further supported by the significant increase in MDA content and significant decrease in GSH content and GSH-Px activity under manganese exposure, while SOD and CAT activities were significantly increased. Simultaneously, the acute manganese stress triggered profound metabolic reprogramming to cope with energy pressure in , which showed that manganese exposure significantly down-regulated energy metabolism-related genes (, , , , , , , ); furthermore, the overall energy metabolism network was widely inhibited, while lipid metabolism-related genes (, ) were significantly up-regulated to compensatorily activate fatty acid transport and β-oxidation pathways. In addition, the acute manganese stress initiated a complex immune response pattern to cope with cell damage in , which showed that manganese exposure significantly enhanced the expression of inflammatory signaling genes (, , ); furthermore, certain inflammatory pathways were activated, while the expressions of immune regulatory genes (, ) were significantly decreased. In summary, these results indicated that manganese exposure could impair immune function, disrupt metabolism, and induce oxidative stress in . - Source: PubMed
Publication date: 2026/03/20
Shen XiaoluWang YongliRen MingchunHuang DongyuGu JiazeZhang LeiminLiang HualiangChen Xiaoru - To investigate the effects of Granules (QSG) on folic acid (FA)-induced renal fibrosis in mice and TGF-β1-stimulated HK-2 cells and the underlying mechanism. - Source: PubMed
Chen YizhenWang WeiliCheng MengZhang WeiGao YilinHong XinZhang LeiDai RongWang Yiping