ALDOB

Last update 08 May 2025

Basic Info

Synonyms

ALDB, ALDOB, aldolase, fructose-bisphosphate B

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Introduction

Catalyzes the aldol cleavage of fructose 1,6-biphosphate to form two triosephosphates dihydroxyacetone phosphate and D-glyceraldehyde 3-phosphate in glycolysis as well as the reverse stereospecific aldol addition reaction in gluconeogenesis. In fructolysis, metabolizes fructose 1-phosphate derived from the phosphorylation of dietary fructose by fructokinase into dihydroxyacetone phosphate and D-glyceraldehyde (PubMed:10970798, PubMed:12205126, PubMed:20848650). Acts as an adapter independently of its enzymatic activity, exerts a tumor suppressor role by stabilizing the ternary complex with G6PD and TP53 to inhibit G6PD activity and keep oxidative pentose phosphate metabolism in check (PubMed:35122041).

100 Clinical Results associated with ALDOB

100 Translational Medicine associated with ALDOB

0 Patents (Medical) associated with ALDOB

334

Literatures (Medical) associated with ALDOB

01 Dec 2025·Rice

A Dual-localized Fructose Bisphosphate Aldolase is Essential for Chloroplast Development and Carbon Metabolism in Rice

Article

Author: Gao, Yingbo ; Yao, Youli ; Zhou, Juan ; Lin, Lingshang ; Zhou, Yong ; Huang, Jianye ; Yang, Zefeng ; Zhang, Xiaoxiang ; Liu, Xin ; Tang, Siyuan ; Ben, Linli ; Dong, Guichun

Fructose-1,6-bisphosphate aldolase (FBA) stands as a pivotal enzyme involved within the Calvin cycle and glycolytic pathways in bacteria and higher plants, but the specific function of OsFBA in rice is still unclear. Here, we identified a chloroplast and mitochondria dual-localized FBA protein, OsFBA1, in rice. Experimental evidence showed that the functionally deficient osfba1 mutants featured a notable decline in chlorophyll content, photosynthetic rate, and severe growth impediment by the three-leaf stage, leading to eventual plant demise. Up-regulation of photosynthetic-pathway genes in the osfba1 mutants indicated the essential role of OsFBA1 in chloroplast development and suggested a compensatory mechanism of other genes in the process. Furthermore, the absence of OsFBA1 impaired the carbon assimilation in young rice seedlings, and supplying exogenous glucose could partially sustain the survival of osfba1 mutant for a few more days. Pathway-specific metabolomics analysis revealed a systemic change of metabolites in the glycolytic pathway, and consequential carbohydrates accumulation due to OsFBA1 disruption. Transcriptomics profiling corroborated the expression changes of photosynthesis, and carbon metabolism pathway genes. We further demonstrated that OsFBA1 serves as the primary FBA enzyme governing energy generation, photosynthesis and carbon metabolism. These results prove that OsFBA1 is an essential core gene in supporting the life cycle of rice, its expression has to be tightly regulated.

01 May 2025·JHEP Reports

Serum proteomics of adults with acute liver failure provides mechanistic insights and attractive prognostic biomarkers

Article

Author: Engel, Bastian ; Hufnagel, Franziska-Maria ; Karkossa, Isabel ; von Bergen, Martin ; Ziegler, Nicole ; Karvellas, Constantine J ; Schubert, Kristin ; Kannt, Aimo ; Krieg, Laura ; Taubert, Richard ; Durkalski-Mauldin, Valerie ; Strnad, Pavel ; Su, Zemin ; Fontana, Robert John ; Luckhardt, Sonja ; Lee, William Martens ; Karl, Anna Sophie ; Remih, Katharina ; Tacke, Frank ; Rule, Jody A ; Tomanová, Petra

Background & AimsAcute liver failure (ALF) is defined as rapid onset coagulopathy and encephalopathy in patients without a prior history of liver disease. We performed untargeted and targeted serum proteomics to delineate processes occurring in adult patients with ALF and to identify potential biomarkers.MethodsSera of 319 adult patients with ALF (∼50% acetaminophen [APAP]-related cases) were randomly selected from admission samples of the multicenter USA Acute Liver Failure Study Group consortium and subdivided into discovery/validation cohorts. They were analyzed using untargeted proteomics with mass spectroscopy and a serum cytokine profiling and compared with 30 healthy controls. The primary clinical outcome was 21-day transplant-free survival. Single-cell RNAseq data mapped biomarkers to cells of origin; functional enrichment analysis provided mechanistic insights. Novel prognostic scores were compared with the model for end-stage liver disease and ALFSG prognostic index scores.ResultsIn the discovery cohort, 117 proteins differed between patients with ALF and healthy controls. There were 167 proteins associated with APAP-related ALF, with the majority being hepatocyte-derived. Three hepatocellular proteins (ALDOB, CAT, and PIGR) robustly and reproducibly discriminated APAP from non-APAP cases (AUROCs ∼0.9). In the discovery cohort, 37 proteins were related to 21-day outcome. The key processes associated with survival were acute-phase response and hepatocyte nuclear factor 1α signaling. SERPINA1 and LRG1 were the best individual discriminators of 21-day transplant-free survival in both cohorts. Two models of blood-based proteomic biomarkers outperformed the model for end-stage liver disease and ALFSG prognostic index and were reproduced in the validation cohort (AUROCs 0.83-0.86) for 21-day transplant-free survival.ConclusionsProteomics and cytokine profiling identified new, reproducible biomarkers associated with APAP etiology and 21-day outcome. These biomarkers may improve prognostication and understanding of the etiopathogenesis of ALF but need to be independently validated.Impact and implicationsAcute liver failure (ALF) is a sudden, and severe condition associated with high fatality. More sensitive and specific prognostic scores are urgently needed to facilitate decision-making regarding liver transplantation in patients with ALF. Our proteomic analysis uncovered marked differences between acetaminophen and non-acetaminophen-related ALF. The identification of routinely measurable biomarkers that are associated with 21-day transplant-free survival and the derivation of novel prognostic scores may facilitate clinical management as well as decisions for/against liver transplantation. Further studies are needed to quantify less abundant proteins. Although we used two cohorts, our findings still need to be independently and prospectively validated.

01 Apr 2025·Metabolism

Fructose-induced progression of steatohepatitis involves disrupting aldolase B-AMPK signaling in methionine adenosyltransferase 1A deficient mice

Article

Author: Millet, Oscar ; Lopitz-Otsoa, Fernando ; Chhimwal, Jyoti ; Fernández-Ramos, David ; Robinson, Aaron E ; Lu, Shelly C ; Luque-Urbano, María ; Van Eyk, Jennifer E ; Barbier-Torres, Lucía ; Mato, José M

OBJECTIVEAldolases (ALDO) are sensors that regulate AMPK via binding to fructose 1,6-biphosphate (FBP), an intermediate of glucose and fructose metabolism. Fructose consumption is linked to metabolic dysfunction-associated steatotic liver disease (MASLD) progression but whether ALDO-AMPK signaling is involved is unknown. Methionine adenosyltransferase alpha 1 (Mat1a) knockout (KO) mice have low hepatic S-adenosylmethionine (SAMe) level and spontaneously develop steatohepatitis. ALDOB methylation has not been reported and here we investigated whether SAMe level regulates ALDOB and ALDOB-AMPK signaling and whether fructose feeding accelerates MASLD progression by disrupting ALDOB-AMPK signaling.METHODSMass spectrometry identified ALDOB methylation sites and recombinant in vitro approaches assessed how methylation at those sites affects ALDOB oligomerization and activity. Primary hepatocytes cultured with high/low glucose and/or fructose and wild type (WT) and Mat1a KO mice fed with a high-fructose diet examined AMPK-ALDOB signaling and MASLD progression.RESULTSIn Mat1a KO livers ALDOB R173 is hypomethylated while ALDOB activity is enhanced. Recombinant ALDOB is methylated at R173 and R304 by protein arginine methyltransferase 1. Low hepatic SAMe level results in hypomethylated ALDOB, which favors the tetrameric form that has higher enzymatic activity, and higher capacity to signal to activate AMPK. Fructose, independently of glucose levels, inhibited AMPK activity and induced lipid accumulation in hepatocytes. Mat1a KO mice have hyperactivated AMPK and fructose feeding inhibits it, enhancing the accumulation of fat in the liver and the progression of MASLD.CONCLUSIONHepatic SAMe levels regulate ALDOB oligomeric state and enzymatic activity impacting on AMPK signaling and fructose-induced MASLD progression.

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ALDOB

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