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    ALDOB aldolase, fructose-bisphosphate B [ Homo sapiens (human) ]

    Gene ID: 229, updated on 17-Sep-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    MRTO4 Enhances Glycolysis to Facilitate HCC Progression by Inhibiting ALDOB.

    MRTO4 Enhances Glycolysis to Facilitate HCC Progression by Inhibiting ALDOB.
    Zheng Y, Huang Y, Li W, Cheng H., Free PMC Article

    07/29/2024
    Associations between ALDOB polymorphisms and intrahepatic cholestasis of pregnancy susceptibility in the Chinese Han population.

    Associations between ALDOB polymorphisms and intrahepatic cholestasis of pregnancy susceptibility in the Chinese Han population.
    Liu X, Xin S, Zheng J, Liu H, Zeng Y, Wu X, Zhang F, Zeng X, Zou Y, Lai H.

    03/21/2024
    Aldolase B-driven lactagenesis and CEACAM6 activation promote cell renewal and chemoresistance in colorectal cancer through the Warburg effect.

    Aldolase B-driven lactagenesis and CEACAM6 activation promote cell renewal and chemoresistance in colorectal cancer through the Warburg effect.
    Chu YD, Cheng LC, Lim SN, Lai MW, Yeh CT, Lin WR., Free PMC Article

    11/2/2023
    Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer.

    Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer.
    Li Y, Tang S, Shi X, Lv J, Wu X, Zhang Y, Wang H, He J, Zhu Y, Ju Y, Zhang Y, Guo S, Yang W, Yin H, Chen L, Gao D, Jin G., Free PMC Article

    09/25/2023
    Aldolase B suppresses hepatocellular carcinogenesis by inhibiting G6PD and pentose phosphate pathways.

    Aldolase B suppresses hepatocellular carcinogenesis by inhibiting G6PD and pentose phosphate pathways.
    Li M, He X, Guo W, Yu H, Zhang S, Wang N, Liu G, Sa R, Shen X, Jiang Y, Tang Y, Zhuo Y, Yin C, Tu Q, Li N, Nie X, Li Y, Hu Z, Zhu H, Ding J, Li Z, Liu T, Zhang F, Zhou H, Li S, Yue J, Yan Z, Cheng S, Tao Y, Yin H.

    04/23/2022
    downregulation of aldolase B and accumulation of fructose 1,6-bisphosphate promote clear cell renal cell carcinoma growth by counteracting oxidative stress

    Accumulation of fructose 1,6-bisphosphate protects clear cell renal cell carcinoma from oxidative stress.
    Wang J, Wu Q, Qiu J.

    06/27/2020
    high ALDOB expression impairs DNA mismatch repair and induces apoptosis in colon adenocarcinoma

    Aldolase B impairs DNA mismatch repair and induces apoptosis in colon adenocarcinoma.
    Lian J, Xia L, Chen Y, Zheng J, Ma K, Luo L, Ye F.

    03/28/2020
    ALDOB knockdown or dietary fructose restriction suppresses growth of colorectal cancer (CRC) liver metastases, but not primary tumors or lung metastases, highlighting the importance of tumor microenvironment.

    Aldolase B-Mediated Fructose Metabolism Drives Metabolic Reprogramming of Colon Cancer Liver Metastasis.
    Bu P, Chen KY, Xiang K, Johnson C, Crown SB, Rakhilin N, Ai Y, Wang L, Xi R, Astapova I, Han Y, Li J, Barth BB, Lu M, Gao Z, Mines R, Zhang L, Herman M, Hsu D, Zhang GF, Shen X., Free PMC Article

    09/21/2019
    Differential gene expression between islets from normoglycemic and hyperglycemic patients was prominent for the glycolytic enzyme ALDOB, mRNA level of ALDOB correlated negatively with insulin secretion and positively with HbA1c. The minor allele of the ALDOB variant rs550915 associated with significantly higher levels of C-peptide and insulin during oral glucose tolerance test and hyperglycemic clamp, respectively.

    The Expression of Aldolase B in Islets Is Negatively Associated With Insulin Secretion in Humans.
    Gerst F, Jaghutriz BA, Staiger H, Schulte AM, Lorza-Gil E, Kaiser G, Panse M, Haug S, Heni M, Schütz M, Stadion M, Schürmann A, Marzetta F, Ibberson M, Sipos B, Fend F, Fleming T, Nawroth PP, Königsrainer A, Nadalin S, Wagner S, Peter A, Fritsche A, Richter D, Solimena M, Häring HU, Ullrich S, Wagner R., Free PMC Article

    09/14/2019
    Silencing Aldolase B activated epithelial markers and repressed mesenchymal markers, indicating inactivation of Aldolase B may lead to inhibition of epithelial-mesenchymal transition

    Aldolase B Overexpression is Associated with Poor Prognosis and Promotes Tumor Progression by Epithelial-Mesenchymal Transition in Colorectal Adenocarcinoma.
    Li Q, Li Y, Xu J, Wang S, Xu Y, Li X, Cai S.

    07/15/2017
    The downregulation of ALDOB could indicate a poor prognosis for HCC patients, and therefore, ALDOB might be considered a prognostic biomarker for HCC, especially at the early stage.

    Aldolase B inhibits metastasis through Ten-Eleven Translocation 1 and serves as a prognostic biomarker in hepatocellular carcinoma.
    Tao QF, Yuan SX, Yang F, Yang S, Yang Y, Yuan JH, Wang ZG, Xu QG, Lin KY, Cai J, Yu J, Huang WL, Teng XL, Zhou CC, Wang F, Sun SH, Zhou WP., Free PMC Article

    05/21/2016
    ALDOC, Aldolase A (ALDOA) and Aldolase B (ALDOB) activate Wnt signaling.

    Aldolase positively regulates of the canonical Wnt signaling pathway.
    Caspi M, Perry G, Skalka N, Meisel S, Firsow A, Amit M, Rosin-Arbesfeld R., Free PMC Article

    07/4/2015
    Single nucleotide polymorphisms in ALDOB, MAP3K1, and MEF2C are associated with cataract.

    Electronic medical records and genomics (eMERGE) network exploration in cataract: several new potential susceptibility loci.
    Ritchie MD, Verma SS, Hall MA, Goodloe RJ, Berg RL, Carrell DS, Carlson CS, Chen L, Crosslin DR, Denny JC, Jarvik G, Li R, Linneman JG, Pathak J, Peissig P, Rasmussen LV, Ramirez AH, Wang X, Wilke RA, Wolf WA, Torstenson ES, Turner SD, McCarty CA., Free PMC Article

    06/27/2015
    both of exogenous and endogenous ALDOB proteins bind to hepatitis B surface antigen and colocalize in the cytoplasm in vitro and inhibit apoptosis of cisplatin-induced HepG2 cells.

    ALDOB acts as a novel HBsAg-binding protein and its coexistence inhibits cisplatin-induced HepG2 cell apoptosis.
    Wu J, Dan C, Zhao HB, Xiao CX, Liu YP, Si LJ, Ren JL, Guleng B.

    04/18/2015
    Efficient inhibition of aldolase B can prevent high glucose-induced overproduction of methylglyoxal and related cellular dysfunction in endothelial cells.

    Aldolase B knockdown prevents high glucose-induced methylglyoxal overproduction and cellular dysfunction in endothelial cells.
    Liu J, Mak TC, Banigesh A, Desai K, Wang R, Wu L., Free PMC Article

    02/23/2013
    Aldolase B with the A149P substitution has activity that is <100-fold that of the wild type.

    Stabilization of the predominant disease-causing aldolase variant (A149P) with zwitterionic osmolytes.
    Stopa JD, Chandani S, Tolan DR., Free PMC Article

    04/16/2011
    These novel mutations in ALDOB represent 2% of alleles in American HFI (hereditary fructose intolerance) patients, with IVS1+1G>C representing a significantly higher allele frequency (6%) among HFI patients of Hispanic and African-American ethnicity.

    Mutations in the promoter region of the aldolase B gene that cause hereditary fructose intolerance.
    Coffee EM, Tolan DR., Free PMC Article

    03/19/2011
    This is the first report of six unrelated patients sharing the same ALDOB deletion, thus indicating a founder effect for this allele.

    Hereditary fructose intolerance: functional study of two novel ALDOB natural variants and characterization of a partial gene deletion.
    Esposito G, Imperato MR, Ieno L, Sorvillo R, Benigno V, Parenti G, Parini R, Vitagliano L, Zagari A, Salvatore F.

    03/5/2011
    Biochemical study of defective aldolase B enzymes is key to revealing the molecular basis of the disease and providing a stronger basis for improved treatment and diagnosis

    The biochemical basis of hereditary fructose intolerance.
    Bouteldja N, Timson DJ.

    07/26/2010
    The five gene transcripts (aldolase B, elafin, MST-1, simNIPhom and SLC6A14) were changed in patients with ulcerative colitis, and were related to the disease activity.

    Five mucosal transcripts of interest in ulcerative colitis identified by quantitative real-time PCR: a prospective study.
    Eriksson A, Flach CF, Lindgren A, Kvifors E, Lange S., Free PMC Article

    01/21/2010
    Sixteen different mutations of the aldolase B (ALDOB) gene were identified in hereditary fructose intolerance patients.

    Hereditary fructose intolerance: frequency and spectrum mutations of the aldolase B gene in a large patients cohort from France--identification of eight new mutations.
    Davit-Spraul A, Costa C, Zater M, Habes D, Berthelot J, Broué P, Feillet F, Bernard O, Labrune P, Baussan C.

    01/21/2010
    Hereditary fructose intolerance with the mutation c.479_482 del AACA

    Clinical and genetic analysis for a Chinese family with hereditary fructose intolerance.
    Chi ZN, Hong J, Yang J, Zhang HJ, Dai M, Cui B, Zhang Y, Gu WQ, Zhang YF, Liu QR, Wang WQ, Li XY, Ning G.

    01/21/2010
    Observational study of genotype prevalence. (HuGE Navigator)

    Aldolase B mutations and prevalence of hereditary fructose intolerance in a Polish population.
    Gruchota J, Pronicka E, Korniszewski L, Stolarski B, Pollak A, Rogaszewska M, Płoski R.

    03/13/2008
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (3) articles

    Increased prevalence of mutant null alleles that cause hereditary fructose intolerance in the American population.
    Coffee EM, Yerkes L, Ewen EP, Zee T, Tolan DR.

    Secreted protein acidic and rich in cysteine (SPARC) gene polymorphism association with hepatocellular carcinoma in Italian patients.
    Segat L, Milanese M, Pirulli D, Trevisiol C, Lupo F, Salizzoni M, Amoroso A, Crovella S.

    Genetic variations in humans associated with differences in the course of hepatitis C.
    Saito T, Ji G, Shinzawa H, Okumoto K, Hattori E, Adachi T, Takeda T, Sugahara K, Ito JI, Watanabe H, Saito K, Togashi H, Ishii K, Matsuura T, Inageda K, Muramatsu M, Kawata S.

    03/13/2008
    there is an important role for physical association between aldolase and the A, B and E subunits of V-ATPase in the regulation of the proton pump

    Physical interaction between aldolase and vacuolar H+-ATPase is essential for the assembly and activity of the proton pump.
    Lu M, Ammar D, Ives H, Albrecht F, Gluck SL.

    01/21/2010
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