Ask about this productRelated 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
- We generated two mouse models, p21 and p21, expressing either telomerase reverse transcriptase (Tert) or a catalytically inactive variant under the control of the p21 promoter. By 18-20 mo of age, ∼15% of mice from both genotypes developed liver tumors with histopathological features resembling human hepatocellular carcinoma (HCC). Whole-exome sequencing identified activating Ctnnb1 mutations and recurrent PP1 subunit alterations in p21 tumors, whereas p21 tumors harbored activating Hras mutations associated with elevated C > A transversions. Both models exhibited chromosomal aberrations commonly observed in human HCC. Transcriptomic analyses revealed that β-catenin-activated tumors recapitulated gene expression signatures of human HCC, whereas MAPK-mutated tumors showed profiles consistent with MAPK/ERK pathway activation. All HCCs suppressed the gluconeogenic genes and , but diverged into two distinct groups based on their glycolytic and target gene expression profiles. Spatial profiling further revealed reduced HNF4α-positive hepatocytes across tumors, independent of HNF4α transcription, and markedly diminished immune cell infiltration, particularly in β-catenin-activated tumors. Collectively, these findings uncover telomere-independent functions of Tert and identify molecular and metabolic features with potential relevance for predicting immunotherapy response. - Source: PubMed
Publication date: 2026/07/02
Braud LauraVernerey JulienGuille ArnaudCordier PierreGinet ClémenceEgger TomBernabe ManuelChurikov DmitriDa Costa QuentinMeghraoui AïdaDesdouets ChantalGu LiBertucci FrançoisLachaud ChristopheGéli Vincent - The metabolic switch between oxidative phosphorylation (OXPHOS) and aerobic glycolysis is a fundamental feature of tumor biology. Its dynamic regulation during pancreatic neuroendocrine tumor (pNET) cell differentiation remains poorly characterized, especially at single-cell resolution. - Source: PubMed
Publication date: 2026/06/09
Yu PingXiao Jin - 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