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Aldolase B also known as fructose-bisphosphate aldolase B or liver-type aldolase is one of three isoenzymes (A, B, and C) of the class I fructose 1,6-bisphosphate aldolase enzyme (EC 4.1.2.13), and plays a key role in both glycolysis and gluconeogenesis.
Fructose-bisphosphate aldolase (EC 4.1.2.13), often just aldolase, is an enzyme catalyzing a reversible reaction that splits the aldol, fructose 1,6-bisphosphate, into the triose phosphates dihydroxyacetone phosphate (DHAP) and glyceraldehyde 3-phosphate (G3P).
Aldolase A (ALDOA, or ALDA), also known as fructose-bisphosphate aldolase, is an enzyme that in humans is encoded by the ALDOA gene on chromosome 16.. The protein encoded by this gene is a glycolytic enzyme that catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate (G3P) and dihydroxyacetone phosphate (DHAP).
Fructose-1-phosphate is metabolized by aldolase B into dihydroxyacetone phosphate and glyceraldehyde. HFI is caused by a deficiency of aldolase B. [5] A deficiency of aldolase B results in an accumulation of fructose-1-phosphate, and trapping of phosphate (fructokinase requires adenosine triphosphate (ATP)). The downstream effects of this ...
11676 Ensembl ENSG00000109107 ENSMUSG00000017390 UniProt P09972 P05063 RefSeq (mRNA) NM_005165 NM_009657 NM_001303423 RefSeq (protein) NP_005156 NP_001290352 NP_033787 Location (UCSC) Chr 17: 28.57 – 28.58 Mb Chr 11: 78.21 – 78.22 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Aldolase C, fructose-bisphosphate (ALDOC, or ALDC), is an enzyme that, in humans, is encoded by the ...
Fructose 1,6-bisphosphate, known in older publications as Harden-Young ester, is fructose sugar phosphorylated on carbons 1 and 6 (i.e., is a fructosephosphate). The β-D-form of this compound is common in cells. [1] Upon entering the cell, most glucose and fructose is converted to fructose 1,6-bisphosphate. [2] [3]
HFI is caused by a deficiency of fructose 1,6-biphosphate aldolase in the liver, kidney cortex and small intestine. Infants and adults are asymptomatic unless they ingest fructose or sucrose. [citation needed] Deficiency of hepatic fructose 1,6-biphosphate (FBPase) causes impaired gluconeogenesis, hypoglycemia and severe metabolic acidemia.
In particular increased fructose-1,6-bisphosphate accumulation can have inhibitory effects on glucose-6-phosphate dehydrogenase, an essential enzyme of this pathway. [6] Lactate accumulation has also been noted in some patients, potentially linked to reciprocal stimulation of pyruvate kinase, a key enzyme in lactic acid fermentation. [8]