Ask about this productRelated genes to: ALDOB Blocking Peptide
- Gene:
- ALDOB NIH gene
- Name:
- aldolase, fructose-bisphosphate B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ALDOB Blocking Peptide
Related articles to: ALDOB Blocking Peptide
- In chronic kidney disease (CKD), there is evidence of loss of function and fibrosis in the progression of tubular epithelial cells; however, the cellular heterogeneity and underlying molecular mechanisms are not well defined. Knowledge of the diversity among tubular cells is essential for precision medicine therapy. - Source: PubMed
Publication date: 2026/04/17
Mao XinhuiWei MinggangLi YilinXia Ping - The TITANIA (mulTi omIcs daTa cANcer dIagnostics therApies) study is an international collaboration to generate high-quality multi-omics cancer profiles. We conducted an exploratory investigation within this framework to understand the molecular basis of lymphovascular invasion (LVI), a critical determinant of metastatic potential in clear cell renal cell carcinoma (ccRCC). We analyzed 31 ccRCC specimens (11 LVI+, 20 LVI-) from the National Cancer Center Hospital East using whole-genome sequencing, RNA sequencing, and proteomic profiling. Our findings were integrated with public single-cell RNA sequencing (GSE159115) and spatial transcriptomics (GSE175540) datasets to provide a broader biological context. LVI+ tumors consistently showed a distinctive hepatic-lineage gene expression signature, with significant upregulation of aldolase B (ALDOB) and other liver-specific metabolism genes at both the RNA and protein levels. Single-cell analysis identified a previously unrecognized hepatic-differentiated tumor subpopulation expressing master transcription factors HNF1A and HNF4A, which was positioned at the terminal stages of tumor evolution. Comparison with established hepatocyte gene signatures from three independent databases confirmed enrichment of hepatic metabolic programs in this subpopulation. Spatial transcriptomics revealed preferential localization within hypoxic tumor regions. A metabolic program resembling hepatic lineage differentiation, associated with aggressive disease features including LVI and hypoxic microenvironments, offers preliminary insights into renal cancer progression and potential biomarker development. This is a discovery-based, hypothesis-generating study; all findings require independent functional validation before clinical application. - Source: PubMed
Yajima ShugoTsukada YuichiroYamashita RiuFujisawa TakaoKuwata TakeshiWatanabe ReikoIshii GenichiroGabelia NinaJuhl HartmutKoga YoshikatsuYoshino TakayukiIto MasaakiMasuda Hitoshi - Pulmonary hypertension (PH) is a life-threatening disorder characterized by progressive pulmonary vascular remodeling, occlusive arteriopathy, and right ventricular failure. However, the molecular mechanisms underlying these pathological hallmarks remain elusive. This study aimed to introduce aldolase B (ALDOB)-K87 lactylation as a critical regulator of mitochondrial fission and metabolic reprogramming in PH pathogenesis. Integrated lactylomic profiling in hypoxic human pulmonary artery smooth muscle cells (PASMCs) and validation in rodent PH models revealed that hypoxia-induced ALDOB-K87 lactylation amplified glycolytic flux, fostering lactate accumulation and self-reinforcing lactylation. Mechanistically, ALDOB lactylation recruited dynamin-related protein 1 (DRP1) to mitochondria via sentrin/SUMO-specific peptidase 3-mediated deSUMOylation of DRP1. This facilitated mitochondrial fragmentation, exacerbating PASMC proliferation, migration, and phenotypic switching. Sirtuin 1 serves as a delactylase for ALDOB, and its downregulation in PH sustains lactylation-driven pathology. Genetic or pharmacological suppression of ALDOB lactylation attenuates mitochondrial fission and PH progression in vivo, whereas lactylation-mimetic mutants exacerbate disease phenotypes. This study unveiled a lactate-ALDOB-DRP1 axis that bridged metabolic rewiring with mitochondrial dynamics, offering novel therapeutic targets for PH. - Source: PubMed
Publication date: 2026/03/27
Yi LiuHe WenmingHe ChangqingShi XianbaoDeng XiaodongChang JinyuNi JieLiu LiShan Lina - It is well recognized that the proteomic plays a critical role in hepatocellular carcinoma (HCC) progression. However, the mechanisms of these proteins, particularly those regulated by phosphorylation, remain incompletely understood. This study aims to systematically characterize stage-specific molecular features of HCC to elucidate the key proteins and post-translational modification (PTM) networks that drive malignant transformation, and to identify candidate core biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/03/11
Sun XueyingHuang HuiZhang QiqiCao XuZhang DuoWang XiaofeiLu XiweiPu Chunwen - Glycogen storage disease type Ia (GSD Ia) is a rare autosomal recessive inherited disorder of carbohydrate metabolism, caused by a deficiency in glucose 6-phosphatase-α (G6PC1). Patients primarily suffer from failure to thrive, hepatomegaly, and severe fasting intolerance, biochemically characterized by hypoketotic, hypoglycemia, and hyperlipidemia. Because of clinical and biochemical heterogeneity, identifying biomarkers is imperative for prognosis and monitoring. An untargeted proteomics workflow was employed for identifying protein changes in liver and plasma from hepatocyte-specific G6pc knockout mice under fed and fasted conditions. This links the effect of hepatic G6Pase/G6pc deficiency to circulating protein biomarkers and allows assessment of the relationship with different clinical circumstances and long-term complications. In the liver, the main differences between hepatic GSD Ia mice versus controls were observed in proteins related to carbohydrate and lipid metabolism, proteasome, ribosome, NAD metabolism, and mitochondria. In GSD Ia mouse plasma, proteins were mainly down-regulated in the complement and coagulation cascades. Effects in hepatic GSD Ia mice were in general more pronounced under fasting conditions. Several potential biomarkers that showed significant alterations in both liver and plasma were identified. These include proteins involved in carbohydrate and lipid metabolism (e.g., UGP2, ALDOB, and FASN), complement and coagulation cascades (SERPINA1E, C8b, and MBL2), 20S proteasome subunits (PSMA4, PSMA7, and PSMB5), and the electron transport chain (SDHA). Their consistent changes observed in both the liver and circulation indicate their potential as circulating biomarkers reflecting liver condition. Together with their reported associations with liver diseases, we hypothesize that they could monitor hepatic complications. - Source: PubMed
Xiao Ruiqide Vries Hilda IGross-Valle CandelasBleeker AychaDerks Terry G JBakker Barbara MOosterveer Maaike HWolters Justina C