Recombinant Human Aldolase C Fructose-Bisphosphate ALDOC
- Known as:
- Recombinant Human Aldolase C Fructose-Bisphosphate ALDOC
- Catalog number:
- enz-085
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Aldolase Fructose-Bisphosphate ALDOC
Related genes to: Recombinant Human Aldolase C Fructose-Bisphosphate ALDOC
- Gene:
- ALDOC NIH gene
- Name:
- aldolase, fructose-bisphosphate C
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-12-04
Related products to: Recombinant Human Aldolase C Fructose-Bisphosphate ALDOC
Related articles to: Recombinant Human Aldolase C Fructose-Bisphosphate ALDOC
- Although there are several proteomic studies testing brain responses to glucocorticoids, there were no attempts to integrate these data and compare them with responses at the level of mRNAs. Furthermore, the utility of available data is compromised by changes in nomenclature and usage of different types of identifiers. Therefore, the aim of this study was to identify the most consistent changes in protein expression in standardized mouse, rat, and human datasets and compare them with transcriptomic responses to glucocorticoids. The analysis showed that the two most frequently and consistently detected proteins were ATP synthase F1 subunit beta (Atp5f1b) and aldolase, fructose-bisphosphate C (Aldoc), while the most consistent proteomic and transcriptomic findings included Aldoc, Plin4, Aqp4, Endod1, Glul, Anln, Aldh1l1, Parp1, Trf, Fermt2, Tmem63a, and Trim2. The study also revealed limitations of available proteomic data indicating significant gaps in knowledge. Finally, the study provides an integrated dataset with updated protein nomenclature and a complete set of major identifiers to facilitate usage of proteomic data. - Source: PubMed
Juszczak Grzegorz R - Obesity is a global epidemic and is the cause of a profound health crisis worldwide. A low-calorie diet (LCD) can alleviate obesity, but the precise mechanisms involved have yet to be thoroughly elucidated. - Source: PubMed
Publication date: 2025/12/24
Chen ShaojunZhang Lihua - Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition with limited effective therapies targeting its underlying biological mechanisms. Acupuncture has shown clinical promise in improving core ASD symptoms, yet its molecular effects remain poorly understood. This study aimed to investigate the systemic mechanisms by which acupuncture exerts therapeutic effects in ASD, using an integrated plasma-based proteomic and metabolomic approach. Twenty children were enrolled, including 10 diagnosed with ASD and 10 age- and sex-matched typically developing controls. The ASD group received a 12-week standardized acupuncture intervention. Plasma samples were collected before and after treatment, and analyzed using data-independent acquisition-based LC-MS/MS for proteomics and high-resolution mass spectrometry for metabolomics. Differentially expressed proteins and metabolites were identified across healthy controls, pre-treatment, and post-treatment ASD groups, followed by pathway enrichment and integrated network analysis. Acupuncture significantly modulated biological pathways related to immune regulation, mitochondrial oxidative phosphorylation, glycolysis, folate biosynthesis, lipid metabolism, and fatty acid degradation. Notable differentially expressed proteins included CD59 and CD5L, ATP5F1A and ALDOC, and HYAL1. Metabolomic profiling revealed altered levels of lipids, lipid-like molecules, benzenoids, and folate-related metabolites, implicating changes in neurochemical balance and detoxification capacity. Fatty acid degradation pathways were also enhanced, suggesting a systemic metabolic shift toward an anti-inflammatory state. Integrating proteomic and metabolomic data, the results support a multi-system mechanism through which acupuncture restores immune-metabolic homeostasis, consistent with the holistic therapeutic framework of traditional Chinese medicine. The identification of candidate biomarkers such as CD59, ATP5F1A, and ALDOC offers potential tools for therapeutic monitoring and mechanistic insight. This study presents the first multi-omics evidence for the biological basis of acupuncture in ASD and provides a rationale for individualized interventions. These findings support future research integrating acupuncture with metabolic, nutritional, or immunological therapies. Larger-scale, controlled trials with functional validation of molecular targets are warranted to confirm these findings and guide clinical translation. - Source: PubMed
Publication date: 2025/11/20
Xu JinboBao Chao - Astrocytes, the most abundant glial cell type in the central nervous system (CNS), are essential for maintaining neural homeostasis, forming gliovascular unit, and modulating synaptic function. However, commonly used astrocytic markers often display regional variability or lack strict specificity, limiting their reliability for consistently identifying astrocytes across brain regions. To address this limitation, we generated a novel transgenic mouse line (AldoC BAC-GFP) that expresses green fluorescent protein (GFP) under the control of the aldolase C (AldoC) promoter using modified bacterial artificial chromosome (BAC) technology. AldoC is an enzyme abundantly expressed in astrocytes. We confirmed that GFP-expressing cells in these mice co-express endogenous AldoC and are co-labeled with established astrocytic markers, thereby validating their astrocytic identity. Importantly, GFP expression was largely restricted to astrocytes throughout diverse brain regions. Moreover, GFP-positive astrocytes in brain slices exhibited the characteristic linear-shaped passive conductance of mature astrocytes. Collectively, these findings demonstrate that AldoC BAC-GFP transgenic mice represent a reliable and broadly applicable model for functional studies of astrocytes in the CNS. - Source: PubMed
Publication date: 2025/12/04
Kim JuhyunYang HayoungKim Seong SeopCho EunsilHer SongHwang Eun MiShim SungboPark Jae-Yong - Oxidative phosphorylation (OXPHOS) is a key player in mitochondrial bioenergetic functions. In hepatocellular carcinoma (HCC), OXPHOS slows down or switches to glycolysis via what is known as the Warburg effect. The altered respiration in cancer was reported to affect mitochondrial temperature. We investigated the impact of the metabolic switch on the mitochondrial temperature in HepG2 HCC cell line. Metformin (N, N-dimethylbiguanide) treatment was used to suppress glycolysis to emulate lower metabolically active cells (Met-HepG2). The mitochondrial temperature was assessed using mito-thermo yellow (MTY) absorbing mitochondrial radiant heat. Mito-tracker green (MTG) fluorescent dye was used to confirm mitochondrial localization. Our data showed lower MTY dye intensity in the Met-HepG2 treated group, indicating a significant increase in mitochondrial temperature compared to untreated HepG2 cells (NT-HepG2). Genotypic analysis of the metabolic respiration gene expression showed significant down-regulation in glycolytic genes (ERR-gamma, HK2, PGK, ALDOC, TPI1, IDH1, and PKM2) in the Met-HepG2 cells compared to the NT-HepG2 cells. OXPHOS as evidenced by ATP, ROS, and NADPH production was significantly up-regulated in the Met-HepG2 group compared to the NT-HepG2 group. Transmission electron microscopy showed fewer mitochondria with swollen elongated appearance, as a marker for activated OXPHOS in the Met-HepG2 group. These data show a correlation between HepG2 altered metabolism and mitochondrial temperature and suggest that less metabolically active HepG2 cells are correlated with higher mitochondrial temperature, providing evidence for a possible role of mitochondrial temperature in diagnosis of HCC. - Source: PubMed
Publication date: 2025/11/21
Gaser Ola ANasr Mohamed AHussein Alaa ESalah Radwa AymanSaad Shams MEhab SeifAboomar Nourhan MElmehrath Ahmed OSalah AymanChang Young-TaeHedrick MalCastanedo Lázaro A MFahimi PeymanMatta Chérif FEl-Badri Nagwa