PEPCK promoter GR EMSA Probe Set
- Known as:
- PEPCK promoter GR EMSA Probe Set
- Catalog number:
- AY1382P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PEPCK promoter EMSA Probe Set
Related genes to: PEPCK promoter GR EMSA Probe Set
- Gene:
- PCK1 NIH gene
- Name:
- phosphoenolpyruvate carboxykinase 1
- Previous symbol:
- -
- Synonyms:
- PEPCK-C
- Chromosome:
- 20q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2015-12-16
- Gene:
- PCK2 NIH gene
- Name:
- phosphoenolpyruvate carboxykinase 2, mitochondrial
- Previous symbol:
- -
- Synonyms:
- PEPCK, PEPCK2
- Chromosome:
- 14q11.2-q12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-04
- Date modifiied:
- 2018-02-13
Related products to: PEPCK promoter GR EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: PEPCK promoter GR EMSA Probe Set
- Mitochondria catabolize nutrients by generating sequentially-ordered organic acid intermediates that are oxidized through the tricarboxylic acid cycle. Pathogenic accumulation of metabolic organic acids manifests as devastating organic acidemias/acidurias and other severe diseases, but the underlying mechanisms are largely unknown. Using unbiased C. elegans genetic screening, we here reveal that mutations in the phosphoenolpyruvate carboxykinases PCK-1 and PCK-2 cause buildup of oxaloacetate, a key tricarboxylic acid cycle intermediate, leading to severe mitochondrial damage. Depletion of mitochondrial GOT-2.1 or GOT-2.2, which catalyze oxaloacetate conversion to aspartate, also causes oxaloacetate accumulation and defective mitochondria with disrupted cristae. We demonstrate that oxaloacetate binds the MICOS complex subunit CHCH-3/MIC19 and inhibits its function of promoting IMMT-1/MIC60-dependent membrane shaping and remodeling. In mammalian cells, aberrant OAA buildup similarly causes mitochondrial impairment through MIC19 and MIC60. These findings not only provide important mechanistic insights into mitochondrial damage in the context of defective oxaloacetate metabolism, but also suggest therapeutic strategies for oxaloacetate-related mitochondriopathies. - Source: PubMed
Publication date: 2026/08/28
Zhang JieShan QianWang XinLi MeijiaoYang YangDuan MeiTang RuofengZhou JunxiangWang FengyangShi YuehuiJiang KaiYang Chonglin - To investigate the source of 3-PG in mouse normal hepatocytes(AML12) under high-Se condition, and to clarify whether the gluconeogenic pathway contributes to SSP activation. - Source: PubMed
Wang JianrongWang QinHan FengXiang XuesongLiu YiqunHuang Zhenwu - Abnormal glucose metabolism often contributes to myofibroblast activation and the pathogenesis of skin fibrotic diseases. All-trans retinoic acid (ATRA), the active component of tretinoin cream, can regulate glucose metabolism and activate myofibroblasts. Importantly, investigating the potential of ATRA to inhibit myofibroblast activation by modulating glucose metabolism could reveal the translational significance of ATRA in attenuating hypertrophic scar (HS) formation. - Source: PubMed
Publication date: 2026/04/27
Li Zi-ChaoZhu Yi-FuSong Ya-JuanTan Zhi-JunLiu BinJiang YanXiao Hou-AnZu Dong-MeiWang TongShi YiJiao YanLi Xue-YongXu Xing-BoShang LeiYu ZhouSong Bao-Qiang - Hemorrhoids are a prevalent condition affecting the anorectal area. Recent studies have highlighted glycolysis as a crucial metabolic pathway in numerous diseases. However, systematic studies exploring the distinct functions of the seven glycolysis-related genes (GRGs) during hemorrhoid development are limited. This investigation sought to elucidate the function of GRGs in hemorrhoid development and their correlation with immune cell infiltration. Using bioinformatics methodologies, we performed differential expression analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, gene set enrichment analysis (GSEA), establishment of protein-protein interaction (PPI) networks, and analysis of immune infiltration. We identified 34 glycolysis-related differentially expressed genes (GRDEGs) in the GSE154650 dataset, including PCK1, ALDOB, and PCK2. GO and KEGG analyses showed a considerable increase of GRDEGs in monosaccharide and glucose metabolic processes and AMPK signaling cascades. PPI network analysis identified seven hub genes (HGs) that may act as essential regulatory nodes and potential drug targets. Additionally, we found notable associations between the infiltration patterns of monocytes and plasma cells and particular HGs, highlighting the significance of the immune microenvironment. This study established a foundation for subsequent functional validation and exploration of innovative therapeutic strategies targeting glycolysis-related pathways in hemorrhoids. - Source: PubMed
Publication date: 2025/09/25
Li PengHou QianYang XiaodongHan WenbinWang Hao - Ferroptosis is a recently identified form of programmed cell death. Increasing studies have suggested the intricate regulation of ferroptosis by metabolic pathways. However, whether gluconeogenesis, a critical branch of glucose metabolism maintaining the dynamic equilibrium with glycolysis, could modulate ferroptosis, remains to be elucidated. Herein, we reported that ferroptotic stress facilitates the expressions of gluconeogenic genes, especially Phosphoenolpyruvate carboxykinase 2 (PCK2). Importantly, ablation of PCK2 substantially enhances ferroptosis susceptibility. This pro-ferroptotic effect is partially attributed to the decreased phosphoenolpyruvate production and occurs independently of mitochondrial stress. Notably, ectopic expression of cytosolic Phosphoenolpyruvate carboxykinase 1 (PCK1) fails to mitigate ferroptosis during PCK2 depletion, suggesting a distinct ferroptosis regulation between PCK1 and PCK2. Therefore, this study highlights a novel ferroptosis regulation by gluconeogenesis, and PCK2 is a potent anti-ferroptotic molecule, although the detailed mechanism remains to be dissected. - Source: PubMed
Publication date: 2025/07/17
Cui HengkangGuo YuboWang XiaohuiLiu LeiWu Hao