1.Biocatalysis of formaldehyde to L-xylose.
Zhailin CHU ; Xiaoyun LU ; Yuwan LIU ; Bo CUI ; Meidong JING ; Huifeng JIANG
Chinese Journal of Biotechnology 2020;36(5):942-948
It is of great significance to use biosynthesis to transform the inorganic substance formaldehyde into organic sugars. Most important in this process was to find a suitable catalyst combination to achieve the dimerization of formaldehyde. In a recent report, an engineered glycolaldehyde synthase was reported to catalyze this reaction. It could be combined with engineered D-fructose-6-phosphate aldolase, a "one-pot enzyme" method, to synthesize L-xylose using formaldehyde and the conversion rate could reach up to 64%. This process also provides a reference for the synthesis of other sugars. With the increasing consumption of non-renewable resources, it was of great significance to convert formaldehyde into sugar by biosynthesis.
Biocatalysis
;
Formaldehyde
;
chemistry
;
Fructose-Bisphosphate Aldolase
;
metabolism
;
Xylose
;
chemical synthesis
2.Angiopoietin-like 4 modulates aldolase A expression in human melanoma cell in a PKC dependent manner.
Yang SUN ; Xiancheng WANG ; Borong FANG ; Xiang XIONG ; Jianhong LONG
Journal of Central South University(Medical Sciences) 2015;40(8):851-857
OBJECTIVE:
To investigate the association between angiopoietin-like 4 (ANGPTL4) and aldolase A (ALDOA) in human melanoma cell.
METHODS:
Overexpression or knockdown of ANGPTL4 was performed in WM-115 or WM-266-4 cells, respectively. The expression of ANGPTL4 and ALDOA was measured by RT-PCR and Western blot, respectively. The promoter activity of ALDOA gene was determined by luciferase assay.
RESULTS:
The promoter activity of ALDOA gene and the expression of ALDOA (mRNA and protein) were increased or decreased in the melanoma cells with overexpression or knockdown of ANGPTL4, which was blocked by selective protein kinase C (PKC) inhibitor or restored by PKC agonist, respectively.
CONCLUSION
ANGPTL4 promotes ALDOA expression in human melanoma cell in a PKC dependent manner.
Angiopoietin-like 4 Protein
;
Angiopoietins
;
genetics
;
metabolism
;
Blotting, Western
;
Cell Line, Tumor
;
Fructose-Bisphosphate Aldolase
;
metabolism
;
Gene Knockdown Techniques
;
Humans
;
Melanoma
;
genetics
;
metabolism
;
RNA, Messenger
;
genetics
;
metabolism
3.A Case of Hereditary Fructose Intolerance.
Dong In KIM ; Eun Sook SUH ; Dong Hwan LEE
Journal of the Korean Child Neurology Society 2000;8(1):94-100
Hereditary fructose intolerance (HFI) is a carbohydrate metabolic disease of autosomal recessive inheritance. The basic deficit is deficiency of aldolase B, the enzyme catalyzing catabolism of fructose-1-phosphate, which is found only in intestinal mucosa, liver and kidney. Its main symptoms are abdominal pain, vomiting, hypoglycemia, and severe liver disease following the ingestion of fructose. Neurologic impairment is not typical in HFI, but it can occur in the acute phase of the disease. Neurologic impairment is related to the acute hepatic toxicity of fructose (hypoglycemia, abnormal coagulation, cardiovascular collapse). The 7 year-old German girl admitted because of generalized tonic clonic seizure. She had the first seizure at the age of 2, and was diagnosed as Lennox-Gastaut syndrome. Thereafter, frequent morning and midnight seizures were developed following indigestion of milk, sweety cake and cookies. Her family history was unknown because she was adopted from India at the 4 months of age. She showed developmental delay. After the ingestion of fructose, the patient experienced hypoglycemic episode within 60-90 minutes of the intake. Based on this finding, she was diagnosed as HFI. With fructose free diet, the patient became free of seizure even without the anticonvulsant, and improved in growth and development.
Abdominal Pain
;
Child
;
Diet
;
Dyspepsia
;
Eating
;
Female
;
Fructose
;
Fructose Intolerance*
;
Fructose-Bisphosphate Aldolase
;
Growth and Development
;
Humans
;
Hypoglycemia
;
India
;
Intestinal Mucosa
;
Kidney
;
Liver
;
Liver Diseases
;
Metabolic Diseases
;
Metabolism
;
Milk
;
Seizures
;
Vomiting
;
Wills
4.Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2.
Mingyue TAN ; Qi PAN ; Qi WU ; Jianfa LI ; Jun WANG
Frontiers of Medicine 2023;17(3):503-517
Aldolase B (ALDOB), a glycolytic enzyme, is uniformly depleted in clear cell renal cell carcinoma (ccRCC) tissues. We previously showed that ALDOB inhibited proliferation through a mechanism independent of its enzymatic activity in ccRCC, but the mechanism was not unequivocally identified. We showed that the corepressor C-terminal-binding protein 2 (CtBP2) is a novel ALDOB-interacting protein in ccRCC. The CtBP2-to-ALDOB expression ratio in clinical samples was correlated with the expression of CtBP2 target genes and was associated with shorter survival. ALDOB inhibited CtBP2-mediated repression of multiple cell cycle inhibitor, proapoptotic, and epithelial marker genes. Furthermore, ALDOB overexpression decreased the proliferation and migration of ccRCC cells in an ALDOB-CtBP2 interaction-dependent manner. Mechanistically, our findings showed that ALDOB recruited acireductone dioxygenase 1, which catalyzes the synthesis of an endogenous inhibitor of CtBP2, 4-methylthio 2-oxobutyric acid. ALDOB functions as a scaffold to bring acireductone dioxygenase and CtBP2 in close proximity to potentiate acireductone dioxygenase-mediated inhibition of CtBP2, and this scaffolding effect was independent of ALDOB enzymatic activity. Moreover, increased ALDOB expression inhibited tumor growth in a xenograft model and decreased lung metastasis in vivo. Our findings reveal that ALDOB is a negative regulator of CtBP2 and inhibits tumor growth and metastasis in ccRCC.
Humans
;
Carcinoma, Renal Cell/genetics*
;
Fructose-Bisphosphate Aldolase/metabolism*
;
Co-Repressor Proteins/metabolism*
;
Transcription Factors/genetics*
;
Kidney Neoplasms/genetics*
;
Cell Line, Tumor
;
Cell Proliferation/genetics*
;
Gene Expression Regulation, Neoplastic
5.Effect of Huanglian Jiedutang on expression of hippocampus proteomics in senescence accelerated mouse.
Shan WANG ; Ning JIANG ; Wen-Xia ZHOU ; Yong-Yiang ZHANG
China Journal of Chinese Materia Medica 2007;32(21):2289-2294
OBJECTIVETo investigate the effect of Huanglian Jiedutang (HLJDT) on hippocampal protein expressions in senescence accelerated mouse-prone/8 (SAMP8).
METHODThe 12-month-old senescence accelerated mice (SAM) were divided into three groups: SAM-resistance/1 (SAMR1), SAM-prone/8 (SAMP8) and SAMP8 treated with HLJDT. The effect of HLJDT on expressions of hippocampal proteins was analyzed by two dimensional electrophoresis (2DE) and matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS).
RESULTCompared with same age SAMR1, there were 29 differential expressed hippocampal proteins in SAMP8. After treated with HLJDT, the expressions of 38 hippocampal proteins of SAMP8 were changed significantly. 12 reactive proteins of HLJDT were chosen to be identified by MALDI-TOF-MS and the results were searched in MASCOT database. Among 12 reactive proteins, the expressions of 4 hippocampal proteins which expressed differentially between SAMR1 and SAMP8 could be improved by HLJDT.
CONCLUSIONHLJDT may improve the aging of SAMP8 by regulating the expressions of proteins related with energy metabolism, signal transduction, cytoskeletal, amino acid metabolism and so on.
Animals ; Coptis ; chemistry ; Drug Combinations ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Electrophoresis, Gel, Two-Dimensional ; Fructose-Bisphosphate Aldolase ; metabolism ; Glutamate-Ammonia Ligase ; metabolism ; Hippocampus ; drug effects ; metabolism ; Male ; Mice ; Plants, Medicinal ; chemistry ; Proteome ; analysis ; metabolism ; Proteomics ; methods ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
6.Anti-cancer activity of Zuojinwan in vivo and influence to tumor markers in mice transplanted with sarcoma 180.
Xiao-Na WANG ; Qin ZHOU ; Xu HAN ; Li-Na XU ; Jin-Yong PENG
China Journal of Chinese Materia Medica 2008;33(19):2230-2234
OBJECTIVETo study the anticancer action of Zuojinwan in mice transplanted with sarcoma 180 in vivo, and detect the activities of five kinds of tumor markers (TM) including acid phosphotase (ACP), alkaline phosphotase (AKP), creatine kinase (CK), aldolase (ALD) and lactate dehydrogenase (LDH) in serum compared with Coptis chinensis and Evodia rutaecarpa.
METHODThe transplanted S180 tumor mice model was established, and the mice were divided randomly five groups. The extract of Zuojinwan (850.8 mg kg(-1)), C. chinensis (729.2 mg kg(-1)) and E. rutaecarpa (121.6 mg kg(-1)) were administrated, respectively for 10 d. Then, the changes of body weight, spleen index of mice, the inhibition rates of tumor, and the increase of life span (ILS) were all tested. In addition, the activities of ACP, AKP, CK, ALD and LDH on different test groups were also determined.
RESULTZuojinwan could inhibit the S180 tumor growth significantly with the inhibition rate of 50.54% and the ILS of mice reached to 64.91%. Meanwhile, the activities of ACP (126.72 +/- 11.16) U 100 mL(-1) and AKP (67.27 +/- 13.49) U 100 mL(-1) were increased, and the activities of CK (20.65 +/- 4.28) U mL(-1), ALD (319.13 +/- 53.87) U L(-1) and LDH (1,029.04 +/- 468.56) U L(-1) were decreased significantly by Zuojinwan treated group compared with C. chinensis and E. rutaecarpa treated groups (P<0.01).
CONCLUSIONIn the prescription of Zuojinwan, the enhancement of compatibility of anticancer activity was observed by the interaction of C. chinensis and E. rutaecarpa. The mechanism might be in according with to influence the activities of the five kinds of tumor markers (TM) in mice serum.
Acid Phosphatase ; blood ; Alkaline Phosphatase ; blood ; Animals ; Antineoplastic Agents ; pharmacology ; Biomarkers, Tumor ; metabolism ; Coptis ; chemistry ; Creatine Kinase ; blood ; Drugs, Chinese Herbal ; pharmacology ; Evodia ; chemistry ; Female ; Fructose-Bisphosphate Aldolase ; blood ; L-Lactate Dehydrogenase ; blood ; Male ; Mice ; Neoplasm Transplantation ; Random Allocation ; Sarcoma 180 ; blood ; drug therapy ; pathology