GPD1 Antibody
- Known as:
- GPD1 Antibody
- Catalog number:
- csb-pa009709ha01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- GPD1 Antibody
Related genes to: GPD1 Antibody
- Gene:
- GPD1 NIH gene
- Name:
- glycerol-3-phosphate dehydrogenase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-11-05
Related products to: GPD1 Antibody
Related articles to: GPD1 Antibody
- To investigate the causal effects of antidiabetic drug targets on Bell's palsy risk using Mendelian randomization (MR), addressing limitations of observational studies and informing therapeutic strategies for diabetic patients. A 2-sample MR analysis was conducted using genetic instruments for 5 major antidiabetic drug classes: sulfonylureas (ABCC8/KCNJ11), metformin (GPD1), thiazolidinediones (PPARG), GLP1-RAs (GLP1R), and SGLTi (SLC5A1/2). Instrumental variables were selected from cis-regions (±500 kb) of target genes using HbA1c-associated single nucleotide polymorphisms (GWAS ID: ebi-a-GCST90014006) with stringent clumping (P < 5 × 10-8, r2 < 0.2) and F-statistic > 10 to ensure robustness. Bell's palsy data were sourced from FinnGen (finn-b-G6_BELLPA) including. Causal effects were assessed via inverse variance weighted, MR-Egger, and weighted median methods, complemented by sensitivity analyses (MR-Pleiotropy RESidual Sum and Outlier, Cochran's Q). Genetically proxied sulfonylurea (via ABCC8/KCNJ11) and metformin (via GPD1) targets exhibited significant protective effects against Bell's palsy, with odds ratios of 0.19 (95% CI: 0.04-0.92, P = .039) and 0.16 (0.03-0.87, P = .034), respectively. Sensitivity analyses confirmed minimal pleiotropy (MR-Egger intercept P > .05) and heterogeneity (Cochran's Q P > .05). No associations were observed for thiazolidinediones, GLP1-RAs, or SGLTi. Scatter plots and inverse variance weighted median concordance supported robustness for ABCC8/KCNJ11, though limited single nucleotide polymorphisms for GPD1 warranted cautious interpretation. This MR analysis provides genetic evidence that sulfonylureas and metformin may confer neuroprotection against Bell's palsy, supporting potential repurposing of these agents to mitigate neurological complications in diabetic patients. - Source: PubMed
Lu KaifuYe LinlinYi XuelianHe Yuxin - Psoriasis is a chronic inflammatory autoimmune skin disease for which no standardised and reliable molecular biomarkers of disease course or activity are currently available. Here, we aimed to identify serum biomarkers of psoriasis. Serum samples from 40 patients with psoriasis and 40 healthy volunteers were analysed using ELISA and Proximity Extension Assay proteomics. ELISA revealed significantly increased serum levels of AGO2 and APOA1 in psoriatic patients versus controls, with a strong association between APOA1 and psoriasis (OR = 20.72, 95% CI of 4.57-93.87, = 0.000137). Targeted serum proteomics additionally identified 35 differentially expressed proteins, including well-known psoriasis drivers (e.g., top upregulated IL17A and SERPINB4). The most downregulated was adrenomedullin (ADM, FC = -10.12). For 14 altered proteins, no previous direct associations with psoriasis were reported. Among them, DEFB103A_DEFB103B and DSG3 showed the best discrimination between psoriasis and control samples, while SERPINB4 correlated with psoriasis severity. APOA1, DEFB103A_DEFB103B, and DSG3 emerge as novel candidate circulating psoriasis biomarkers, and SERPINB4 as a biomarker of psoriasis severity. The functional role of DSG3 and other newly identified proteins (ACRV1, HAO1, ADH4, GPD1, GFER, PTGES2, DSG3, AFAP1L1, GALNT3, RASGRP2, MAP2K6, LXN, NBEAL2, and VPS54) in psoriasis requires further studies. - Source: PubMed
Publication date: 2026/06/26
Dźwigała MonikaSys DorotaŻycka-Krzesińska JoannaRybicka BeataPopławski PiotrWalecka-Herniczek IrenaPiekiełko-Witkowska AgnieszkaBogusławska Joanna - Esophageal squamous cell carcinoma (ESCC) is a malignancy characterized by a poor prognosis, with dysregulated lipid metabolism and chromatin remodeling playing critical roles in its pathogenesis. Small nucleolar RNAs (snoRNAs) represent a conserved family of non-coding RNAs, primarily recognized for their role in directing post-transcriptional modifications of ribosomal RNAs (rRNAs), such as 2'-O-methylation and pseudouridylation. In this study, we identified a conserved H/ACA box snoRNA, SNORA11B, significantly downregulated in ESCC tissues and patient serum samples. Functionally, SNORA11B exerts tumor-suppressive effects by inhibiting proliferation and migration of ESCC cells and promoting apoptosis. Mechanistically, through RNA pulldown assays coupled with mass spectrometry, we identified SMARCA4, a core ATPase subunit of the SWI/SNF chromatin remodeling complex, as a direct interactor of SNORA11B. We further demonstrated that SNORA11B facilitates the recruitment of SMARCA4 to the GPD1 promoter region. This recruitment increases chromatin accessibility for the transcription factor C/EBPβ, thereby enabling transcriptional activation of GPD1. The subsequent upregulation of GPD1 leads to glycerol-3-phosphate (G3P) accumulation, which induces mitochondrial compromise, ultimately contributing to the suppression of tumor progression. Clinically, high expression of SNORA11B is significantly associated with favorable prognosis in ESCC patients. Moreover, its detectable stability in serum, together with a high area under the curve (AUC) value, highlights its promising utility as a novel diagnostic biomarker. Our findings reveal a non-canonical role of SNORA11B as an epigenetic regulator and underscore the SNORA11B/GPD1 axis as a promising diagnostic target for ESCC. SNORA11B recruits SMARCA4 to the GPD1 promoter, enhancing chromatin accessibility and facilitating C/EBPβ-mediated GPD1 transcription. This leads to mitochondrial dysfunction and suppresses esophageal squamous cell carcinoma progression. - Source: PubMed
Publication date: 2026/07/07
Hu LanLu WeiqingHuang ZikunLiu DongchenChen XinruiMa XinlingLiu ZhaoyongZhang Ying - Efficient methane (CH) conversion remains challenging because of the inert C-H bond and the complexity of the multistep reaction process. Herein, we designed and fabricated a C/ZnO/Pd photocatalyst for the selective methane oxidation to C products, achieving a C production rate of 55.1 mmol·g·h and 11,020 mmol·g·h, with a selectivity of up to 98%. Mechanistic studies reveal that the high performance arises from a directional charge transfer strategy enabled by the synergistic integration of Pd and the carbon layer. The carbon layer provides a carbon-mediated electron-transfer channel, while the Pd interface introduces a Pd-mediated hole-transfer pathway. These two components work in concert to promote directional charge transfer and suppress reverse migration. This asymmetric charge behavior further gives rise to a spatially cooperative pathway for methane conversion and oxygen activation. The generality of this strategy is supported by extending it to different metal active sites and an alternative route for constructing the carbon layer. This work provides a strategy for designing high-performance photocatalysts for methane valorization. - Source: PubMed
Publication date: 2026/07/07
Zhang HongnaSong YundongZhang RuixueYu LiangliangChen BoqiangShi JialeHuang YuZheng JimingJiang Hai-Ying - Although abolishing the Crabtree effect in Saccharomyces cerevisiae through a pyruvate dehydrogenase bypass eliminates carbon loss through ethanol overflow metabolism, it compromises growth rates. While the Crabtree effect has been a valuable natural adaptation, it is energetically inferior to respiration and is generally undesirable in cell factories engineered to produce assimilatory compounds. Restoring growth efficiency in Crabtree-negative strains remains a central challenge. Through adaptive laboratory evolution of the engineered strain (sZJD23) and subsequent reverse engineering, a variant (sZJD28) with markedly improved growth was identified. This improvement is driven primarily by a mutation in MED2 (encoding a Mediator complex subunit) and, to a lesser extent, a mutation in GPD1 (encoding glycerol-3-phosphate dehydrogenase). By integrating quantitative proteomics with enzyme-constrained genome-scale modelling, we demonstrate that these mutations jointly enable a more efficient mode of oxidative stress adaptation and energy utilization. The GPD1 mutation suppresses a protein-costly, suboptimal NAD⁺-recycling strategy reliant on glycerol synthesis, while the MED2 mutation reshapes the oxidative stress response towards peroxisomal detoxification. Collectively, these adjustments optimize metabolic flux distribution and reduce protein costs in energy metabolism, thereby increasing ATP availability. Our findings reveal how coordinated mutations in regulatory and metabolic genes restore growth fitness in engineered Crabtree-negative yeast. - Source: PubMed
Publication date: 2026/06/21
Tafur Rangel AlbertCastillo García AndrésMalina CarlSiewers VerenaKerkhoven Eduard J