PGK1 Antibody
- Known as:
- PGK1 Antibody
- Catalog number:
- csb-pa00035a0rb
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- PGK1 Antibody
Related genes to: PGK1 Antibody
- Gene:
- PGK1 NIH gene
- Name:
- phosphoglycerate kinase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xq21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-10-05
Related products to: PGK1 Antibody
Related articles to: PGK1 Antibody
- Histone lactylation is an epigenetic modification triggered by lactate produced during glycolysis. In cancer, histone lactylation can coordinate metabolic and epigenetic states to promote tumor development and progression. Here, we identified circ2891 as a driver of metabolic reprogramming and histone lactylation in colorectal cancer (CRC). In patients, circ2891 was aberrantly upregulated in tumors and correlated with poor outcomes. Elevated circ2891 potentiated aerobic glycolysis and lactate production in CRC cells, supporting enhanced cell proliferation and tumor growth. Mechanistically, circ2891 specifically interacted with the m6A reader FXR1 and facilitated its phase separation, which stabilized PGK1 and ENO1 mRNAs by enhancing the recognition of their m6A modification sites. Consequently, elevated PGK1 and ENO1 led to increased aerobic glycolysis and drove histone lactylation, thereby transcriptionally activating the RNA helicase DDX21 to promote CRC progression. Simultaneously targeting circ2891 and histone lactylation suppressed patient-derived organoid and xenograft tumor growth. Together, these findings show that circ2891 promotes CRC by stabilizing PGK1/ENO1 via phase separation of FXR1, boosting glycolysis and histone lactylation to activate expression of DDX21. Targeting circ2891 offers a promising therapeutic strategy enhancing clinical outcomes. - Source: PubMed
Publication date: 2026/08/05
Jiang TaoLiu JianquanHu QihangQi JunwenLiu BowenMa NingXu YixinZhang LongChen JunnanSong Jun - Metabolic reprogramming and immune regulation are tightly interconnected processes that critically influence cancer progression. The efficacy of immunotherapy is limited in triple-negative breast cancer (TNBC) by metabolic abnormality and immunosuppressive microenvironment. However, the molecular mechanisms through which these alterations cooperate to drive immune evasion and tumor progression in TNBC remain poorly defined. Through transcriptomic profiling, we identified glycolysis and chemokine signaling as the dominant intersecting metabolic and immune pathways that distinguish TNBC from non-TNBC subtypes. Phosphoglycerate kinase 1 (PGK1) is associated with poor prognosis and with myeloid-derived suppressor cells (MDSCs), acting as a key metabolic node linking metabolic regulation to immune modulation. Functionally, PGK1 knockdown inhibited tumor growth in vitro and in vivo and reduced MDSC recruitment. Notably, PGK1 knockdown exerted a more pronounced antitumor effect under immune surveillance, accompanied by decreased infiltration of both monocytic and polymorphonuclear MDSCs and recovered CD8 T cell function. Mechanistically, PGK1 increased lactate production and global lysine lactylation. Notably, histone H3 lysine 18 lactylation (H3K18la) at the CCL5 promoter served as a dominant and required epigenetic modification for PGK1-driven CCL5 transcription, thereby driving CCL5-dependent MDSC recruitment. P300 and class I HDACs were identified as candidate "writer" and "eraser" enzymes for PGK1-dependent H3K18la modification. Notably, combining the PGK1 inhibitor ABT-E79 with anti-PD-1 therapy synergistically decreased MDSC infiltration, recovered CD8 T cell function, and elicited superior antitumor responses compared to monotherapy. Collectively, this study shows a mechanistic link between metabolic reprogramming and immune evasion, offering new therapeutic insights for TNBC. Starting from analyzing metabolic and immunological signaling pathways in cancers lacking clear therapeutic targets and treatment options, we aimed to identify metabolism-associated regulators of immune responses as potential therapeutic targets. Focusing on triple-negative breast cancer (TNBC), through transcriptomic profiling, we identified glycolysis and chemokine signaling as the dominant intersecting metabolic and immune pathways that distinguish TNBC from non-TNBC subtypes. Functional assays demonstrated that PGK1-driven glycolysis in TNBC cells promotes lactate accumulation and H3K18la, which subsequently induce transcriptional activation of CCL5 and recruitment of MDSCs, thereby impairing CD8 T cell function and fostering an immunosuppressive tumor microenvironment that facilitates immune evasion. Furthermore, treatment with ABT-E79, a PGK1 inhibitor, enhances the antitumor immune efficacy of anti-PD-1 therapy. - Source: PubMed
Publication date: 2026/08/04
Wang Yong-PengDang Wen-ZhenLiu Zhen-DanLi BingXiong HuanBai HudagulaLi XiaoWu ShuoLuo ChengXiao Wei-LieZhang Yuan-Yuan - Polycystic ovary syndrome (PCOS) is a common endocrine disorder with developmental origins. While the etiology is unclear, current postulates include epigenetic programming. Cell-type-specific epigenetic changes by which prenatal androgen excess programs the neuroendocrine axis have not been defined. Using single-nucleus (sn) multiome sequencing (snRNAseq + snATACseq) of the mouse preoptic area, we profiled transcriptional and chromatin accessibility landscapes across 31 cell populations on postnatal day 18-22 in a prenatal androgenization (PNA) mouse model that produces neuroendocrine phenotypes that resemble hyperandrogenemic PCOS. Marker gene analysis identified 17 neuronal and 14 non-neuronal populations. We refined the GnRH neuron cluster to 41 neurons by manual curation. Cross-dataset comparisons were used to characterize the molecular transcriptional identity of these clusters. Gene set enrichment analysis of mRNA expression data revealed enrichment of protein synthesis and oxidative phosphorylation pathways and suppression of TNF/NF-κB signaling and steroid responsiveness across several clusters in PNA animals. Pseudobulk differential chromatin accessibility testing across ∼30,600 peaks identified 15 false discovery rate-significant differentially accessible regions, including two loci in GnRH neurons at genomic regions of unknown function, suggesting prenatal androgen exposure changes chromatin accessibility in this and other cell types. Chromosome accessibility at most sex steroid receptor genes was surprisingly present in GnRH neurons. Reduced Pgk1 promoter accessibility in multiple glial populations suggests PNA alters epigenetic regulation of glial energy metabolism. These findings support a model of developmental programming in which prenatal androgen exposure produces cell-type-specific changes that include but are not limited to epigenetic remodeling to generate the PNA phenotype. - Source: PubMed
Publication date: 2026/08/01
Burger Laura LChikodikar Rujuta MMoenter Suzanne M - Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD), are progressive disorders with limited therapeutic options. Centella asiatica (C. asiatica), a medicinal and edible plant, has been reported to exert neuroprotective and anti-neuroinflammatory properties. Yet, the mechanisms underlying its effects against neurodegenerative diseases remain largely unclear. - Source: PubMed
Publication date: 2026/07/31
Xie YuxiLim Chong-TeikLam Xin-JiehCheah Pike-SeeLing King-HwaHuang Tan - Edgew. is a traditional Tibetan medicinal plant used to treat nephritis and edema; however, its active constituents and the molecular mechanisms underlying its renoprotective properties remain poorly elucidated. This study investigated the pharmacological activity and mechanism of Boeravinone A (BA), a major constituent of , in lipopolysaccharide (LPS)-induced acute kidney injury (AKI). A mouse model of LPS-induced AKI and LPS-stimulated RAW264.7 macrophages were used to evaluate the anti-inflammatory and renoprotective effects of BA in vivo and in vitro. Activity-based protein profiling (ABPP) was performed to identify potential molecular targets, followed by validation using isothermal titration calorimetry (ITC), cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) assays. The functional role of the identified target was further examined using shRNA-mediated knockdown and virtual knockout analysis. BA dose-dependently attenuate LPS-induced renal injury and reduced inflammatory responses. Phosphoglycerate kinase 1 (PGK1) was identified as a direct target of BA. Mechanistically, BA activated the Kelch-like ECH-associated protein 1-nuclear factor erythroid 2-related factor 2 (Keap1-Nrf2) pathway through PGK1, enhanced the expression of antioxidant enzymes such as , and reduced the production of pro-inflammatory cytokines, including IL-1β and IL-6. Virtual knockout of PGK1 in macrophages further supported its regulatory role in this pathway. These findings suggest that BA exerts renoprotective effects by targeting PGK1 and activating the Keap1-Nrf2 pathway, thereby reducing oxidative stress and inflammation. This study provides a pharmacological basis for the traditional use of and supports BA as a potential candidate for mechanism-based intervention in AKI. - Source: PubMed
Publication date: 2026/07/20
Lan YiAi LunqiongTang LiqingWang NanZhan HonghongYuan HanChen Min