Редактирование: ACMSD

2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (EC 4.1.1.45) (Picolinate carboxylase)

==Publications==

{{medline-entry
|title=De novo NAD  synthesis enhances mitochondrial function and improves health.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30356218
|abstract=Nicotinamide adenine dinucleotide (NAD ) is a co-substrate for several enzymes, including the sirtuin family of NAD -dependent protein deacylases. Beneficial effects of increased NAD  levels and sirtuin activation on mitochondrial homeostasis, organismal metabolism and lifespan have been established across species. Here we show that α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase ([[ACMSD]]), the enzyme that limits spontaneous cyclization of α-amino-β-carboxymuconate-ε-semialdehyde in the de novo NAD  synthesis pathway, controls cellular NAD  levels via an evolutionarily conserved mechanism in Caenorhabditis elegans and mouse. Genetic and pharmacological inhibition of [[ACMSD]] boosts de novo NAD  synthesis and sirtuin 1 activity, ultimately enhancing mitochondrial function. We also characterize two potent and selective inhibitors of [[ACMSD]]. Because expression of [[ACMSD]] is largely restricted to kidney and liver, these inhibitors may have therapeutic potential for protection of these tissues from injury. In summary, we identify [[ACMSD]] as a key modulator of cellular NAD  levels, sirtuin activity and mitochondrial homeostasis in kidney and liver.
|mesh-terms=* Animals
* Caenorhabditis elegans
* Carboxy-Lyases
* Cell Line
* Choline
* Conserved Sequence
* Disease Models, Animal
* Evolution, Molecular
* Female
* Gene Knockdown Techniques
* Health
* Hepatocytes
* Homeostasis
* Humans
* Kidney
* Liver
* Longevity
* Male
* Methionine
* Mice
* Mice, Inbred C57BL
* Mitochondria
* NAD
* Non-alcoholic Fatty Liver Disease
* Rats
* Sirtuins

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448761
}}