Редактирование: NMNAT3

Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 3 (NMN/NaMN adenylyltransferase 3) (Nicotinamide-nucleotide adenylyltransferase 3) (NMN adenylyltransferase 3) (Nicotinate-nucleotide adenylyltransferase 3) (EC 2.7.7.18) (NaMN adenylyltransferase 3) (Pyridine nucleotide adenylyltransferase 3) (EC 2.7.7.1) (PNAT-3) [FKSG76]

==Publications==

{{medline-entry
|title=Restoration of Mitochondrial NAD  Levels Delays Stem Cell Senescence and Facilitates Reprogramming of Aged Somatic Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27428041
|abstract=The fundamental tenet that aging is irreversible has been challenged by the development of reprogramming technology that can restore molecular and cellular age by reversing the progression of aging. The use of cells from aged individuals as sources for reprogramming or transplantation creates a major barrier in stem cell therapy with respect to cell quality and quantity. Here, we investigated the molecular features underlying senescence and rejuvenation during aged cell reprogramming and identified novel factors that can overcome age-associated barriers. Enzymes, such as nicotinamide nucleotide transhydrogenase ([[NNT]]) and nicotinamide mononucleotide adenylyltransferase 3 ([[NMNAT3]]), that control mitochondrial NAD  levels appear to be susceptible to aging. In aged cells, mitochondrial NAD  levels decrease, accompanied by reduced [[SIRT3]] activity; these changes severely impede cell fate transition. However, in cells collected from aged p16 knockout mice, which exhibit delayed cellular senescence, no changes in [[NNT]] or [[NMNAT3]] expression were found. Importantly, restoring mitochondrial NAD  levels by overexpressing [[NNT]] and [[NMNAT3]] enhanced reprogramming efficiency of aged somatic cells and extended the lifespan of human mesenchymal stem cells by delaying replicative senescence. These results demonstrate that maintenance of mitochondrial NAD  levels is critical for reversing the mechanisms of aging and ensuring that cells collected from aged individuals are of high quality. Stem Cells 2016;34:2840-2851.
|mesh-terms=* Aging
* Animals
* Cell Lineage
* Cellular Reprogramming
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p16
* Gene Knockdown Techniques
* Humans
* Mesenchymal Stem Cells
* Mice, Knockout
* Mitochondria
* NAD
* NADP Transhydrogenases
* Nicotinamide-Nucleotide Adenylyltransferase
* Sirtuin 3
* Stem Cells
|keywords=* Aging
* Mitochondria
* NAD
* Nicotinamide mononucleotide adenylyltransferase 3
* Nicotinamide nucleotide transhydrogenase
|full-text-url=https://sci-hub.do/10.1002/stem.2460
}}