Ask about this productRelated genes to: BPGM Blocking Peptide
- Gene:
- BPGM NIH gene
- Name:
- bisphosphoglycerate mutase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-11-27
Related products to: BPGM Blocking Peptide
Related articles to: BPGM Blocking Peptide
- This study seeks to investigate the underlying mechanism of glycolytic key gene bisphosphoglycerate mutase (BPGM) in nonalcoholic fatty liver disease (NAFLD). qRT-PCR and immunohistochemistry were utilized to detect BPGM levels in clinical NAFLD samples. HepG2 cells and liver organoids were treated with free fatty acid. (FFA). The role of BPGM in NAFLD was explored at cellular, organoid, and animal levels. Metabolomics was performed to analyze differential metabolites and metabolic pathways. Furthermore, we examined the regulatory mechanisms of BPGM by HIF-1α in NAFLD. Results indicated that high expression of BPGM in NAFLD samples was correlated with NAFLD progression. Moreover, Severe group had higher BPGM expression than Mild group. FFA treatment induced time-dependent steatosis and BPGM upregulation in HepG2 cells and liver organoids, whereas BPGM knockdown attenuated lipid accumulation, cellular injury, and oxidative stress. At the animal level, knockdown of BPGM reversed high-fat diet (HFD) induced lipid accumulation and liver tissue injury. Metabolomics studies showed significant changes of metabolic pathways including glycolysis/gluconeogenesis and pyruvate metabolism. Verification experiment showed FFA increased pyruvic acid levels, and knockdown of BPGM decreased pyruvic acid levels. Pyruvic acid further reversed the changes in NAFLD progression caused by BPGM knockdown at the cellular and organoid levels. Finally, HIF-1α regulated the expression of BPGM in NAFLD. Together, our findings suggest that BPGM contributes to abnormal glucose metabolism and promotes hepatic steatosis, thereby driving NAFLD progression. - Source: PubMed
Publication date: 2026/05/13
Zhou ZhengZheng XiyanChen XianqingXie MaoyunDu FeiLin ZhiqunShi Xianjie - Steroid-induced osteonecrosis of the femoral head (SONFH) is a major cause of disability among young and middle-aged adults. However, current diagnosis relies primarily on imaging findings and clinical manifestations, as stable and reliable molecular biomarkers for adjunctive diagnosis and risk stratification remain lacking, thereby hindering timely and effective intervention. Aberrant lactate metabolism is thought to contribute to the onset and progression of various inflammatory diseases by reshaping the inflammatory microenvironment and reprogramming immune responses. However, its role and regulatory mechanisms in SONFH remain understudied. In this study, we analyzed transcriptomic data from SONFH patients in the GEO database, integrating differential expression analysis with weighted gene co-expression network analysis (WGCNA) to identify SONFH-associated genes and co-expression modules. Cross-screening with lactate-related genes (LRGs) curated in the MSigDB database yielded a set of LRGs closely associated with SONFH. Unsupervised consensus clustering was then applied to stratify patients into molecular subtypes, and a machine-learning-based diagnostic model was constructed. In parallel, gene set variation analysis (GSVA) and CIBERSORT were used to characterize metabolic states and immune cell infiltration across subtypes, with a focus on LRGs implicated in metabolic reprogramming and immune dysregulation. Finally, bone marrow-derived mesenchymal stem cells (BMSCs) were collected from Sprague-Dawley rats and humans, along with peripheral blood from patients, and in vitro experiments confirmed significant downregulation of BPGM, FBXL4, and RHAG in SONFH, genes closely linked to bone metabolic imbalance and immune microenvironment remodeling. Collectively, these findings systematically elucidate the potential molecular regulatory role of LRGs in SONFH and provide a theoretical basis for its auxiliary diagnosis and the development of targeted therapeutic strategies. - Source: PubMed
Wang ZehuaDong ShuhangXu KaigeTang XinyuGuo SijiaJiang YapingZhang YingzeLi Tao - Clear cell renal cell carcinoma (ccRCC) is characterized by profound metabolic reprogramming and limited responsiveness to therapeutic stressors, including epigenetic modulation. How glycolytic enzymes contribute to metabolic stress tolerance in ccRCC remains incompletely understood. We investigated the role of the glycolytic enzyme 2,3-bisphosphoglycerate mutase (BPGM) using human tumor specimens, siRNA-mediated gene silencing, functional cell-based assays, and transcriptomic profiling. Epigenetic stress was induced using Vorinostat as a pan-histone deacetylase inhibitor. BPGM expression was consistently elevated in human ccRCC compared with adjacent normal kidney tissue. A498 cells exhibited high basal BPGM levels and limited sensitivity to Vorinostat, whereas BPGM depletion increased cellular stress responses and reduced proliferative capacity. Despite similar phenotypic outcomes, silencing and Vorinostat treatment triggered distinct transcriptional programs. While HDAC inhibition induced widespread transcriptional changes, BPGM loss elicited a focused stress-associated response, consistent with activation of the unfolded protein response, increased lipid peroxidation, and induction of ER stress-associated genes. Our data identify BPGM as a metabolic player contributing to stress-adaptive transcriptional states in ccRCC and suggest that targeting metabolic stress adaptation may complement epigenetic strategies in renal cancer. - Source: PubMed
Publication date: 2026/03/31
Becker Philipp NKulow Vera ACzopek Claudia SRoegner KameliyaTer-Avetisyan GoharLoth AnicaNitzsche BiancaErdogan CemSchreiber AdrianHöpfner MichaelFähling MichaelLabes Robert - Research shows that patients with viral pneumonia complicated by diabetes have a worse prognosis and higher mortality. Our study aimed to assess the effect of diabetes on respiratory tract microbes and the transcriptome in patients with viral pneumonia. We included 76 subjects from China-Japan Friendship Hospital, including 16 healthy people, 17 patients with viral pneumonia and diabetes (VD), and 43 patients with viral pneumonia without diabetes (VP). We collected their sputum samples for both metagenomic and 16S rRNA sequencing and collected blood samples for RNA sequencing. In transcriptome analysis, the VD group downregulated the expression of PTCH1 and upregulated the expression of ANK1, RBM38, BPGM, CRYM, TAL1, and HBD. The differential pathways are mainly reflected in the formation, development, and maintenance of red blood cells, the activity of immunoglobulins, and the membrane transport and transportation of substances. There is a significant difference in microbial diversity between the two groups. Both analysis methods demonstrate a significant increase in the abundance of , and in the VP group. The host genes AGAP1, RNF182, and ANKRD9 are particularly closely associated with microorganisms. Our results suggest that diabetes may inhibit the expression of genes related to immune regulation, energy metabolism, and oxygen utilization in patients with viral pneumonia. Meanwhile, we predict that VD may be associated with a decrease in microbial diversity and a decline in microbial functions in cellular processes, environmental adaptation, metabolism, and genetic activity. These abnormalities can worsen the course of viral pneumonia and affect the prognosis of patients. - Source: PubMed
Publication date: 2026/04/06
Huang ChangruiFeng QinqiYu BangZou HaoCai YashiLiu JianLi DeminZhang HongchunZou Xiaohui - Metabolic adaptations that fuel metastatic dissemination are increasingly mapped, yet the existence of intrinsic metabolic "brakes" that actively restrain metastatic progression remains enigmatic. Here, we unveil bisphosphoglycerate mutase (BPGM) as a previously unrecognized metastasis suppressor that orchestrates a phospho-epigenetic relay linking glycolytic flux to carnitine-dependent fatty acid oxidation. Through high-resolution metabolomics, we discover that BPGM and its catalytic product 2,3-bisphosphoglycerate (2,3-BPG) constitute a metabolic checkpoint whose disruption predicts metastatic virulence in multiple cancers. Mechanistically, BPGM suppresses metastasis by triggering CDK1-T phosphorylation-dependent assembly of an EZH2-H3K27me3 repressor complex that silences γ-butyrobetaine hydroxylase (BBOX1), the rate-limiting enzyme in carnitine biosynthesis. This phospho-switch mechanism converts glycolytic 2,3-BPG levels into epigenetic orchestrator, thereby starving metastatic cells of carnitine-required fatty acid oxidation. Hypoxia-mediated KDM4A-H3K9me3 cascade emerges as the upstream inactivator of this metabolic-epigenetic checkpoint, explaining how tumor microenvironmental stress liberates metastatic potential. Therapeutically, pharmacological BBOX1 inhibition with Meldonium recapitulates BPGM-mediated metastasis suppression in orthotopic models, reducing metastatic burden. These findings reveal BPGM as a metabolic gatekeeper that integrates bioenergetic sensing with chromatin remodeling to constrain metastatic competence, while hypoxia-mediated checkpoint failure unleashes carnitine-fueled metastatic progression. Targeting the hypoxia-BPGM-BBOX1 axis represents an innovative approach for metastasis-preventive therapy. - Source: PubMed
Publication date: 2026/03/23
Wu Meng-ZhiFeng DouLiu Wu-PingHuang Wei-LunWu QiangChou Tian-ShengXiao Wen-HaoYao Zhou-ZhouLi Zhen-JiangXie Ting-TingChen Chang-HanYang Zhi-YuMao Rui-WenWu Ci-ChunWang Jun-ChengZhang Yu-JinKellems Rodney EXia Yang