Disease relevance of Acmsd

• The rat ACMSD ORF was inserted into a mammalian expression vector, before transfection into human hepatoma HepG2 cells [1].

High impact information on Acmsd

• ACMSD cDNAs isolated from liver and kidney were shown to be identical, consisting of a 1008 bp open reading frame (ORF) encoding 336 amino acid residues with a molecular mass of 38091 Da [1].
• Expression of rat hepatic 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase is affected by a high protein diet and by streptozotocin-induced diabetes [2].
• In the tryptophan-niacin conversion, 2-amino-3-carboxymuconate-6-semiardehyde decarboxylase (ACMSD; formerly termed picolinic carboxylase) is an important enzyme regulating the generation of quinolinate [2].
• Hepatic alpha-amino-beta-carboxymuconate-e-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis from tryptophan [3].
• The aim of this study was to evaluate the ACMSD mRNA expression after pyrazinamide or peroxisome proliferators ingestion [3].

Biological context of Acmsd

• Therefore, in this study, we examined whether dietary linoleic acid altered ACMSD gene expression and its protein level [4].
• Since liver ACMSD activity in adrenalectomized rats was also increased by feeding a high-protein diet, adrenocortical hormone was thought to be unnecessary for such enzyme induction [5].
• In tryptophan-niacin metabolism, alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) [EC 4.1.1.45] is known to play an important role by catalyzing the decarboxylation of alpha-amino-beta-carboxymuconate-epsilon-semialdehyde, a metabolite of tryptophan which cyclizes spontaneously to form quinolinate [5].

Associations of Acmsd with chemical compounds

• However, pyrazinamide does not affect the transcription level of hepatic ACMSD [3].
• Shifting from the control diet to a clofibrate diet suppressed ACMSD mRNA strongly at day 1 and continued through day 4 [3].
• In rats fed with several kinds of peroxisome-proliferator-containing diets such as phthalate ester, bezafibrate, Wy-14,643, 2-(-4-chlorophenoxy) propionic acid, or dehydroisoandrosterone for 8 days, hepatic ACMSD mRNA was drastically decreased by all the peroxisome proliferators [3].
• The results indicated that the induction of hepatic ACMSD activity by diabetes was not due to removal of the suppressive effect of the linoleic acid on the enzyme [6].
• Moreover, this study provides the information that a high polyunsaturated fatty acid diet affects the production of quinolinic acid in serum by suppressing the ACMSD activity [7].

Analytical, diagnostic and therapeutic context of Acmsd

• Purification and molecular cloning of rat 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase [1].
• The distribution of ACMSD mRNA expression in various tissues was investigated in the rat by RT-PCR [1].
• In diabetic rats, hepatic ACMSD activity was higher in the fat free diet group than in the linoleic acid group [6].
• Therefore, in this study, we examined the differential effect of fatty acids on ACMSD mRNA expression by Northern blot [7].
• Hepatic ACMSD activity in the D-galN-injected group was lower than that of the control group [8].

References