ALDOB antibody
- Known as:
- ALDOB (anti-)
- Catalog number:
- orb101228
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ALDOB antibody
Related genes to: ALDOB antibody
- 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 antibody
Related articles to: ALDOB antibody
- This study investigated the effects of environmentally relevant concentrations of deoxycorticosterone acetate (DOCA) on embryonic development and oxidative stress in zebrafish (Danio rerio), while also elucidating the underlying molecular mechanisms. Embryos were exposed to DOCA at 5, 50, and 500 ng/L, spanning both environmentally pertinent and elevated concentrations. Integrated morphological and transcriptomic analyses (RNA-seq and qRT-PCR) demonstrated dose-dependent acceleration of development, along with alterations in pigmentation, oxidative balance, and metabolic processes. At 50 ng/L, yolk extension increased by 43.3 %, whereas yolk sac area decreased by 3.28 %. At 500 ng/L, these effects intensified (yolk extension: 44.4 %; yolk sac area: -5.28 %). Body pigmentation decreased by 13.7 % compared to controls at 500 ng/L. At 5 ng/L, ROS levels and MDA content increased by 66.5 % and 53.4 %, respectively. Transcriptomic profiling at 16 h post-fertilization in embryos exposed to 500 ng/L DOCA identified significant gene expression changes concordant with phenotypic outcomes: (1) upregulation of six7, sox17, and cdx1a (associated with accelerated development); (2) downregulation of dct and slc45a2 (consistent with reduced pigmentation); (3) altered redox homeostasis, indicated by nox1 upregulation and hemoglobin gene downregulation; and (4) enhanced glycolytic/gluconeogenic activity, evidenced by upregulated pfkfb3, aldob, and pck2. These results demonstrate that the DOCA exposure perturbed embryonic zebrafish development, promoting accelerated morphogenesis concurrent with metabolic alterations and oxidative stress. This study provides the first evidence of DOCA's adverse effects on fish and advances understanding of understudied corticosteroids in ecotoxicology. - Source: PubMed
Publication date: 2025/10/28
Liu ShenaoWang KaifengHuang WenweiZhang JiemingHan ChongLi QiangGong Jian - Carrier screening is a long-standing genetic testing process offered to at-risk couples, with or without a family history, who might have pregnancies affected by an autosomal recessive (AR) or X-linked (XL) disorder. A total of 276 unrelated individuals, initially referred for rare disorder screening by clinicians, were enrolled in this study and tested by Exome sequencing (ES). Expanded carrier screening (ECS) was performed for 176 disorders that met the inclusion criteria of the ACMG and ACOG. Genes with single nucleotide variants (SNVs) identified with a carrier rate > 1% for AR disorders included HBB, CFTR, PMM2, NPHS2, GJB2, ACADM, ALDOB, MEFV, MKS1, NEB, PAH, ATM, CPT2, CYP21A2, AGXT, BBS1, CAPN3, COL4A4, DHCR7, GAA, IVD, LAMA2, SLC22A5, SLC26A4, USH2A. For XL disorders, variants were detected in the RS1 gene. ECS offers a wealth of information about SNVs related to AR and XL disorders in specified populations. The information obtained from ECS provides multiple advantages: (a) it identifies the most prominent risks in health care in a given population and contributes to the prevention of genetic disorders, (b) it enriches available databases with pathogenic or likely pathogenic SNVs, and (c) it records novel targets for molecular clinical genetic testing. - Source: PubMed
Publication date: 2026/05/29
Kostoulas CharilaosSesse AthanasiaBouba IoannaNajdecki RobertKonitsiotis SpyridonMarkoula SofiaGeorgiou Ioannis - Hereditary fructose intolerance is a rare but potentially severe and fatal disorder if it is not recognized promptly. It is caused by biallelic mutations in the gene, which encodes the Aldolase B enzyme. Deficiency leads to intracellular accumulation of fructose-1-phosphate, causing secondary inhibition of gluconeogenesis and glucogenolysis and, consequently, hypoglycemia along with hepatic and renal dysfunction. The clinical presentation is variable and often nonspecific, making diagnosis challenging. - Source: PubMed
Publication date: 2026/05/26
Carrillo Michelle HigueraTamayo Sara VallejoSandoval Melquisedec Vargas - This study investigated how chronic heat stress affects meat quality and post-slaughter muscle acidification in slow-growing yellow-feathered broilers, focusing on the roles of ALDOB and HSP90B1 in glycometabolism. From 100 to 120 days of age, broilers were kept either under thermoneutral conditions (25 ± 1 °C, N group) or cyclic heat stress (32 ± 1 °C for 9 h/day, H group). Meat quality traits (pH, shear force, drip loss, color) were measured at 0, 24, and 48 h of refrigeration (4 °C). Free amino acid and fatty acid profiles were analyzed. DF-1 cells were exposed to 43 °C for functional assays of and . Chronic heat stress reduced body weight, altered flavor precursors, and induced PSE-like characteristics (lower pH, higher shear force, increased drip loss, paler color), especially in leg muscles. and were upregulated in both tissues and cells. overexpression promoted glucose consumption, while suppressed lactic acid production. Chronic heat stress impairs growth and flavor precursors and exacerbates post-slaughter muscle acidification (primarily driven by ATP hydrolysis, with lactic acid as a secondary contributor). and may dually regulate glycometabolism under heat stress. - Source: PubMed
Publication date: 2026/04/27
Xu YongjieWeng ZhuoxianHuang XunheChao XiaohuanZhang XiquanZhang XiaonanLuo Qingbin - Fructose consumption increases the risk of obesity-related metabolic diseases and some cancers, but its role in hepatocellular carcinogenesis (HCC) remains controversial. Animal studies suggest that high fructose promotes HCC, whereas human data fail to support the positive link between fructose intake and elevated risk of liver cancer. Moreover, fructose metabolism is progressively attenuated in HCC with the loss of key fructolytic enzymes, including fructose-1,6-bisphosphate aldolase B (ALDOB). Here, we report that fructose suppresses HCC through fructose 1-phosphate (F1P)-mediated inhibition of mannose phosphate isomerase (MPI) in the context of ALDOB deficiency. Transcriptomic and metabolic flux analyses using human HCC cells and tissues revealed that liver cancer cells retain a significant ability to metabolize fructose despite the downregulation of fructolytic genes, with ALDOB showing the earliest and most pronounced suppression compared with GLUT2 and KHK. Dietary supplementation with 10% fructose suppressed HCC in liver-specific Aldob knockout mice. Further spatial and single-cell transcriptomic analyses of clinical HCC samples revealed the spatiotemporal dynamics of fructolytic gene expression and identified subsets of cancer cells that retain fructose uptake and phosphorylation capacity (SLC2A2⁺/KHK⁺) but lack ALDOB expression. Upon fructose exposure, accumulated F1P binds to and inhibits MPI, reducing protein N-glycosylation and triggering apoptosis due to maladaptive ER stress. We further performed virtual high-throughput screening of FDA-approved and clinical-trial drugs and identified ebselen as a potent MPI inhibitor. Taken together, the results of our study reveal a novel mechanism by which dietary fructose inhibits HCC through the F1P-MPI axis, suggesting a therapeutic strategy targeting metabolic vulnerabilities in cancer. - Source: PubMed
Publication date: 2026/05/25
Wang YongqiangZhang XiangyangWang NingningJiang HuiminLiang NingningDu ChenxiYin ChunzhaoLi RuiZhang LiliTu QiaochuLv JingwenMa HaoranXu XiaodongKong XinranChen XinLiu GuijunChen ShitingXu HualingQin JunLi ShengxianTao YongzhenZeng ShanShen HongGoncalves Marcus DZhong ShanshanYin Huiyong