Ask about this productRelated genes to: PDHB antibody
- Gene:
- PDHB NIH gene
- Name:
- pyruvate dehydrogenase E1 beta subunit
- Previous symbol:
- -
- Synonyms:
- PDHE1B
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2017-08-08
Related products to: PDHB antibody
Related articles to: PDHB antibody
- Mitochondrial dysfunction is an emerging metabolic hallmark of age-related diseases, yet tools to directly profile mitochondrial pathways and test metabolic interventions in the living human eye remain limited. Multi-omics ocular liquid biopsy enables real-time proteomic and metabolomic profiling of the intraocular microenvironment, complementing systemic biomarkers and imaging surrogates. Here, we used this approach to define mitochondrial and tricarboxylic acid (TCA) cycle dysregulation in geographic atrophy (GA) and to assess whether oral α-ketoglutarate (α-KG) supplementation can modulate mitochondrial metabolites within the eye. - Source: PubMed
Publication date: 2026/03/19
Yeh Tsai-ChuVelez GabrielPrasad ArchiteshLee Soo HyeonRasmussen Ditte KKumar AarushiChadha MadhumeetaDabaja Mohamed ZiadSingh Aneal MSanislo StevenSmith StephenMryuthyunjaya PrithviMontague ArtisBassuk Alexander GAlmeida DavidDufour AntoineMahajan Vinit B - Glioblastomas (GBM) are highly aggressive, treatment-resistant brain tumors lacking clinically actionable, noninvasive prognostic biomarkers. Tumor response after standard-of-care chemoradiation (CRT) is difficult to interpret on imaging, and post-CRT MRI changes have not been well linked to molecular features or potential biomarkers. - Source: PubMed
Publication date: 2026/03/18
Krauze AndraNguyen TrinhSierk MichaelJackson LukeChappidi ShreyaChen QingrongYan ChunhuaHu YingHarmon StephanieTasci ErdalCooley TheresaSproull MaryMackey MeganMeerzaman DaoudCamphausen Kevin - Pulmonary fibrosis (PF), a progressive interstitial lung disease with elusive pathogenesis, remains a therapeutic challenge. Emerging evidence suggests cuproptosis-a copper-dependent cell death pathway-may play a regulatory role in disease progression. This study aims to elucidate cuproptosis's biological function and establish a prognostic model for PF. Through integrative analysis of single-cell RNA-seq data from bleomycin (BLM)-induced mouse models and bulk RNA-seq data from idiopathic pulmonary fibrosis (IPF) patients, we identified cuproptosis-related genes (CRGs) using LASSO regression and Cox regression. A novel 4-CRG signature (LIAS, LIPT1, ATP7A, PDHB) was constructed to stratify patients into distinct risk groups in the GSE70866 cohort, where high-risk individuals exhibited poorer survival and enhanced extracellular matrix/lipid metabolism activity via GO/KEGG analysis. Experimental validation in BLM-induced mouse models, TGF-β1-stimulated fibroblast-to-myofibroblast transition assays, and human IPF specimens demonstrated significant downregulation of CRGs through qRT-PCR and immunohistochemical analyses. Functional assays revealed impaired cell viability and elevated cuproptosis markers in fibrotic microenvironments. Our findings establish an inverse correlation between cuproptosis and PF progression, and propose a robust risk-score model for clinical prognosis prediction. This multi-omics approach provides new insights into copper-mediated regulatory mechanisms in fibrogenesis. - Source: PubMed
Publication date: 2026/03/13
Chen MengtingChen JialuZhang JiaxiangZhu YongMeng XiaoxiaoYang ZhengfengWang Ruilan - A 6 month subchronic toxicity study demonstrated that exposure to the mineral oil saturated hydrocarbon (MOSH) subfraction (predominant carbon range C) induced dose- and gender-dependent immunometabolic disruption in Fischer 344 rats. Both low- (1.5 g/kg) and high-dose (15 g/kg) exposure significantly reduced the arterial blood CD4/CD8 T-cell ratio in both genders (female: 1.85 ± 0.40 and 1.27 ± 0.13 vs 3.14 ± 0.20 in controls; male: 1.04 ± 0.39 and 0.95 ± 0.26 vs 4.38 ± 0.54 in controls), indicating concomitant immune dysregulation and inflammation. Integrated metabolomic and proteomic analyses of the spleen elucidated distinct gender-associated responses. Females exhibited upregulated purine metabolism, evidenced by elevated purine intermediates (5-aminoimidazole ribonucleotide and 5'-phosphoribosyl--formylglycinamide) and increased expression of proteins involved in de novo synthesis (PRPS1, GART, and ADSS2) and salvage pathways (adenylate kinase 3, guanine deaminase, and GMPR). In contrast, males displayed a dual pathophysiological pattern characterized by systemic purine activation alongside suppressed mitochondrial energy metabolism (PDHB, HK1, and ACSS1), impaired glutathione homeostasis (GSR and GSTA4), and downregulated heme metabolism (ALAS2, HMBS, CPOX, FECH, HMOX1, and CP). These alterations were consistently more pronounced in the high-dose group. The findings reveal gender-specific immunometabolic toxicity of the MOSH C subfraction, highlighting the necessity of incorporating gender-specific effects and immunometabolic endpoints in future risk assessment of MOSH exposure. - Source: PubMed
Publication date: 2026/02/27
Zhu LinZhang MingmingZhang HongZhang HaiGao BoyanYu Liangli LucyZhang Yaqiong - Cell fate determination is closely linked to metabolic state, yet how metabolic remodeling influences human pluripotent stem cells differentiation into three germ layers remains incompletely understood. Here, we reveal that definitive endoderm differentiation from human pluripotent stem cells requires a TGFβ-driven metabolic switch characterized by reduced lactate production and enhanced TCA cycle activity and oxidative phosphorylation, mediated by PDHB. Disruption of glucose utilization or pyruvate entry into the TCA cycle markedly impairs endoderm differentiation, whereas inhibition of lactate production enhances differentiation efficiency. Mechanistically, blockade of glucose metabolism or the TCA cycle reduces intracellular ATP levels, compromising the activity of BAF complex, an ATP-dependent chromatin remodeling complex centered on BRG1. This complex promotes chromatin accessibility and activates endodermal gene programs during differentiation. Together, these findings highlight metabolic reprogramming as a key regulator of human endoderm fate through ATP-dependent control of chromatin remodeling. - Source: PubMed
Publication date: 2026/02/17
Meng LimingLv JingYi YingLan XianchunYan ChenchaoZhu LihangYang JieJiang Wei