| Nmnat1 Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1. | Nmnat1 Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1.
Hasegawa K, Tamaki M, Sakamaki Y, Wakino S., Free PMC Article | 07/16/2024 |
| Nuclear Nicotinamide Adenine Dinucleotide Deficiency by Nmnat1 Deletion Impaired Hepatic Insulin Signaling, Mitochondrial Function, and Hepatokine Expression in Mice Fed a High-Fat Diet. | Nuclear Nicotinamide Adenine Dinucleotide Deficiency by Nmnat1 Deletion Impaired Hepatic Insulin Signaling, Mitochondrial Function, and Hepatokine Expression in Mice Fed a High-Fat Diet.
Dong H, Guo W, Yue R, Sun X, Zhou Z., | 03/26/2024 |
| Adipocyte NMNAT1 expression is essential for nuclear NAD[+] biosynthesis but dispensable for regulating thermogenesis and whole-body energy metabolism. | Adipocyte NMNAT1 expression is essential for nuclear NAD(+) biosynthesis but dispensable for regulating thermogenesis and whole-body energy metabolism.
Yamaguchi S, Kojima D, Iqbal T, Kosugi S, Franczyk MP, Qi N, Sasaki Y, Yaku K, Kaneko K, Kinouchi K, Itoh H, Hayashi K, Nakagawa T, Yoshino J. | 11/28/2023 |
| Deletion of Nmnat1 in Skeletal Muscle Leads to the Reduction of NAD[+] Levels but Has No Impact on Skeletal Muscle Morphology and Fiber Types. | Deletion of Nmnat1 in Skeletal Muscle Leads to the Reduction of NAD(+) Levels but Has No Impact on Skeletal Muscle Morphology and Fiber Types.
Karim M, Iqbal T, Nawaz A, Yaku K, Nakagawa T. | 07/6/2023 |
| Loss of hepatic Nmnat1 has no impact on diet-induced fatty liver disease. | Loss of hepatic Nmnat1 has no impact on diet-induced fatty liver disease.
Iqbal T, Nawaz A, Karim M, Yaku K, Hikosaka K, Matsumoto M, Nakagawa T. | 11/19/2022 |
| The mouse nicotinamide mononucleotide adenylyltransferase chaperones diverse pathological amyloid client proteins. | The mouse nicotinamide mononucleotide adenylyltransferase chaperones diverse pathological amyloid client proteins.
Huang C, Lu J, Ma X, Qiang J, Wang C, Liu C, Fang Y, Zhang Y, Jiang L, Li D, Zhang S., Free PMC Article | 06/11/2022 |
| Mutant Nmnat1 leads to a retina-specific decrease of NAD+ accompanied by increased poly(ADP-ribose) in a mouse model of NMNAT1-associated retinal degeneration. | Mutant Nmnat1 leads to a retina-specific decrease of NAD+ accompanied by increased poly(ADP-ribose) in a mouse model of NMNAT1-associated retinal degeneration.
Greenwald SH, Brown EE, Scandura MJ, Hennessey E, Farmer R, Du J, Wang Y, Pierce EA., Free PMC Article | 04/2/2022 |
| Nuclear NAD(+)-biosynthetic enzyme NMNAT1 facilitates development and early survival of retinal neurons. | Nuclear NAD(+)-biosynthetic enzyme NMNAT1 facilitates development and early survival of retinal neurons.
Sokolov D, Sechrest ER, Wang Y, Nevin C, Du J, Kolandaivelu S., Free PMC Article | 01/29/2022 |
| An Alu-mediated duplication in NMNAT1, involved in NAD biosynthesis, causes a novel syndrome, SHILCA, affecting multiple tissues and organs. | An Alu-mediated duplication in NMNAT1, involved in NAD biosynthesis, causes a novel syndrome, SHILCA, affecting multiple tissues and organs.
Bedoni N, Quinodoz M, Pinelli M, Cappuccio G, Torella A, Nigro V, Testa F, Simonelli F, TUDP (Telethon Undiagnosed Disease Program), Corton M, Lualdi S, Lanza F, Morana G, Ayuso C, Di Rocco M, Filocamo M, Banfi S, Brunetti-Pierri N, Superti-Furga A, Rivolta C. | 08/21/2021 |
| SARM1 depletion rescues NMNAT1-dependent photoreceptor cell death and retinal degeneration. | SARM1 depletion rescues NMNAT1-dependent photoreceptor cell death and retinal degeneration.
Sasaki Y, Kakita H, Kubota S, Sene A, Lee TJ, Ban N, Dong Z, Lin JB, Boye SL, DiAntonio A, Boye SE, Apte RS, Milbrandt J., Free PMC Article | 02/20/2021 |
| The present study found that Nmnat1 is essential for the early development of the retina, particularly for the survival of retinal progenitor cells that are fated to retinal subtypes in the inner nuclear layer. | Roles of Nmnat1 in the survival of retinal progenitors through the regulation of pro-apoptotic gene expression via histone acetylation.
Kuribayashi H, Baba Y, Iwagawa T, Arai E, Murakami A, Watanabe S., Free PMC Article | 11/16/2019 |
| We propose that the E257K allele is a weak hypomorphic allele that has significantly reduced penetrance in the homozygous state. In contrast, compound heterozygous Nmnat1(E257K/-) mice exhibit photoreceptor defects which are exacerbated upon exposure to light. | NMNAT1 E257K variant, associated with Leber Congenital Amaurosis (LCA9), causes a mild retinal degeneration phenotype.
Eblimit A, Zaneveld SA, Liu W, Thomas K, Wang K, Li Y, Mardon G, Chen R., Free PMC Article | 01/12/2019 |
| that increasing NMNAT1 levels can slow the progression of symptoms and neuropathological features of tauopathy | NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy.
Rossi F, Geiszler PC, Meng W, Barron MR, Prior M, Herd-Smith A, Loreto A, Lopez MY, Faas H, Pardon MC, Conforti L., Free PMC Article | 08/11/2018 |
| Using steady-state and flux analysis of NAD(+) metabolites in healthy and injured mouse dorsal root ganglion axons, we find that rather than altering NAD(+) synthesis, NMNAT1 instead blocks the injury-induced, SARM1-dependent NAD(+) consumption that is central to axon degeneration. | NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD(+) depletion.
Sasaki Y, Nakagawa T, Mao X, DiAntonio A, Milbrandt J., Free PMC Article | 11/25/2017 |
| Mouse-non nuclear-nicotinamide mononucleotide adenylyltransferase type 1 maintains mitochondrial nicotinamide levels and thereby supports mitochondrial unfolded protein response function and mitochondrial proteostasis in injured neurons. | Nicotinamide mononucleotide adenylyltransferase promotes hypoxic survival by activating the mitochondrial unfolded protein response.
Mao XR, Kaufman DM, Crowder CM., Free PMC Article | 12/17/2016 |
| NMNAT1 overexpression enhanced AMPK activity in oxygen-glucose deprivation treated cortical neurons | Nicotinamide Mononucleotide Adenylyltransferase 1 Protects Neural Cells Against Ischemic Injury in Primary Cultured Neuronal Cells and Mouse Brain with Ischemic Stroke Through AMP-Activated Protein Kinase Activation.
Liang J, Wang P, Wei J, Bao C, Han D. | 03/12/2016 |
| An increased level of Nmnat protein in hiw mutants is both required and sufficient to inhibit axonal degeneration. | The Highwire ubiquitin ligase promotes axonal degeneration by tuning levels of Nmnat protein.
Xiong X, Hao Y, Sun K, Li J, Li X, Mishra B, Soppina P, Wu C, Hume RI, Collins CA., Free PMC Article | 05/25/2013 |
| Overexpression of Nmnat1 in the cytoplasm and axons of RGCs robustly protected against both ischemic and glaucomatous loss of RGC axonal integrity, as well as loss of RGC soma. | Protection of mouse retinal ganglion cell axons and soma from glaucomatous and ischemic injury by cytoplasmic overexpression of Nmnat1.
Zhu Y, Zhang L, Sasaki Y, Milbrandt J, Gidday JM., Free PMC Article | 02/23/2013 |
| Findings reveal a novel role for NMNAT1 in the morphogenesis of developing cortical neurons, which indicate that the loss of function of NMNAT1 may contribute to different neurodegenerative disorders in central nervous system. | Nicotinamide mononucleotide adenylyltransferase 1 gene NMNAT1 regulates neuronal dendrite and axon morphogenesis in vitro.
Zhao H, Zhang JY, Yang ZC, Liu M, Gang BZ, Zhao QJ. | 05/5/2012 |
| Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death. | Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death.
Verghese PB, Sasaki Y, Yang D, Stewart F, Sabar F, Finn MB, Wroge CM, Mennerick S, Neil JJ, Milbrandt J, Holtzman DM., Free PMC Article | 01/28/2012 |
| NMNAT1 is indispensable for the normal development of the embryo. Decreased NMNAT1 activity in heterozygous null mice does not affect the rate of Wallerian degeneration, suggesting that endogenous NMNAT1 does not have a primary role in axon maintenance. | Reducing expression of NAD+ synthesizing enzyme NMNAT1 does not affect the rate of Wallerian degeneration.
Conforti L, Janeckova L, Wagner D, Mazzola F, Cialabrini L, Di Stefano M, Orsomando G, Magni G, Bendotti C, Smyth N, Coleman M. | 09/17/2011 |
| nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons blocks axonal degeneration | Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons.
Sasaki Y, Milbrandt J., Free PMC Article | 02/26/2011 |
| Through NAMPT activity, visfatin contributes to vascular inflammation, causing atherothrombotic diseases linked to metabolic disorders. | Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity.
Romacho T, Azcutia V, Vázquez-Bella M, Matesanz N, Cercas E, Nevado J, Carraro R, Rodríguez-Mañas L, Sánchez-Ferrer CF, Peiró C. | 05/3/2010 |
| This study provided the evidence that Nmnat1 protein manifest robust delay in axonal degeneration. | Transgenic mice expressing the Nmnat1 protein manifest robust delay in axonal degeneration in vivo.
Sasaki Y, Vohra BP, Baloh RH, Milbrandt J., Free PMC Article | 01/21/2010 |
| results suggest that axonal protection by NMNAT expression in neurons is provided by modifying mitochondrial function | Nicotinamide mononucleotide adenylyltransferase expression in mitochondrial matrix delays Wallerian degeneration.
Yahata N, Yuasa S, Araki T., Free PMC Article | 01/21/2010 |