The NAD+ Synthesis Enzyme Nicotinamide Mononucleotide Adenylyltransferase (NMNAT1) Regulates Ribosomal RNA Transcription

Song, Tanjing; Yang, Leixiang; Kabra, Neha; Koomen, John M.; Haura, Eric B.; Chen, Jiandong

doi:10.1074/jbc.m113.470302

Cited by 42 publications

(50 citation statements)

References 33 publications

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“…The axon protection conferred by NMNAT1 seems to be closely related to mitochondria, which is a critical organelle for the maintenance of redox state (59,60). In addition, NMNAT1 also has other functional implications (50,59,(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78).…”

Section: Discussionmentioning

confidence: 99%

Targeted deletion of Nmnat1 in mouse retina leads to early severe retinal dystrophy

Wang

Fang

Liao

et al. 2017

Preprint

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Mutations in NMNAT1 can lead to a very severe type of retinal dystrophy, Leber congenital amaurosis, in human patients, characterized by infantile-onset or congenital retinal dystrophy and childhood blindness. The loss-of-function mouse models of Nmnat1 have not been well-established, since the complete knock-out (KO) of Nmnat1 in mice results in embryonic lethality. Here, we generated retina-specific KO by using the Crxpromotor-driving Cre combined with the flox allele. By a panel of histological and functional analyses, we found that Nmnat1 conditional KO (cKO) mice have early severe retinal dystrophy. Specifically, the photoreceptors of Nmnat1 cKO mice are almost diminished and the retinal functions also become completely abolished. Our results established a loss-of-function model for Nmnat1 in mice, which will be useful for studying the detailed functions of NMNAT1 in the retina.peer-reviewed)

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Section: Discussionmentioning

confidence: 99%

Targeted deletion of Nmnat1 in mouse retina leads to early severe retinal dystrophy

Wang

Fang

Liao

et al. 2017

Preprint

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“…Indeed, it is directly involved in multiple DNA repair pathways, and it modulates the transcription of several metabolic genes to mediate cell adaptation to nutrient/energy stress [5,6]. Activation of these enzymes is strictly dependent on the availability of their shared cosubstrate NAD, and, indeed, the same stress conditions have also been shown to stimulate the expression of NAD biosynthetic enzymes, like nicotinamide phosphoribosyltransferase and NMN adenylyltransferase-1 [7][8][9][10][11][12]. In lower eukaryotes, e.g.…”

Section: Introductionmentioning

confidence: 99%

NAD homeostasis in the bacterial response to DNA/RNA damage

2014

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“…Current studies indicate that both Maf1 and nicotinamide mononucleotide adenylyltransferase (NMNAT1), a positive effector of eNoSC activity, may function as tumor suppressors. Maf1 expression is diminished in human liver cancers [32, 35] while the NMNAT1 locus frequently undergoes heterozygous deletion in human cancers [60]. The ability of Maf1 to control intracellular lipids further suggests that it may also be dysregulated in metabolic diseases, although studies are necessary to assess this possibility.…”

Section: Resultsmentioning

confidence: 99%