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NMNAT1 encodes an enzyme which catalyzes a key step in the biosynthesis of the coenzyme NAD. Additionally we are shipping NMNAT1 Proteins (19) and NMNAT1 Kits (3) and many more products for this protein.
Showing 10 out of 54 products:
Human Monoclonal NMNAT1 Primary Antibody for EIA, WB - ABIN567609
Zhang, Berrocal, Frizzell, Gamble, DuMond, Krishnakumar, Yang, Sauve, Kraus: Enzymes in the NAD+ salvage pathway regulate SIRT1 activity at target gene promoters. in The Journal of biological chemistry 2009
Show all 3 references for ABIN567609
Chicken Polyclonal NMNAT1 Primary Antibody for WB - ABIN2783549
Sorci, Cimadamore, Scotti, Petrelli, Cappellacci, Franchetti, Orsomando, Magni: Initial-rate kinetics of human NMN-adenylyltransferases: substrate and metal ion specificity, inhibition by products and multisubstrate analogues, and isozyme contributions to NAD+ biosynthesis. in Biochemistry 2007
Hidden Genetic Variation in LCA9-Associated Congenital Blindness Explained by 5'UTR (show UTS2R Antibodies) Mutations and Copy-Number Variations of NMNAT1.
We confirmed a diagnosis of NMNAT1-associated Leber congenital amaurosis in two siblings through identification of the mutation (c.25G>A [p. Val9Met]) in a homozygous state.
NMNAT1, which encodes the nicotinamide mononucleotide adenylyltransferase 1, has been recently identified to be one of the LCA (show CLTA Antibodies)-causing genes. Our results expanded the spectrum of mutations in NMNAT1
To study how mutations affect NMNAT1 function and ultimately lead to a retinal degeneration phenotype, we performed detailed analysis of Leber congenital amaurosis 9-associated NMNAT1 mutants.
theNMNAT1 p.Glu257Lys variant is a hypomorphic variant that almost without exception causes leber congenital amaurosis (LCA (show CLTA Antibodies)) in combination with more severe NMNAT1 variants.
The aim of this study was to determine the occurrence and frequency of NMNAT1 mutations and associated phenotypes in different types of inherited retinal dystrophies.
Data found pathogenic DNA variants in the genes RP1 (show STK19 Antibodies), USH2A (show USH2A Antibodies), CNGB3 (show CNGB3 Antibodies), NMNAT1, CHM (show CHM Antibodies), and ABCA4 (show ABCA4 Antibodies), responsible for retinitis pigmentosa, Usher syndrome, achromatopsia, Leber congenital amaurosis, choroideremia (show CHM Antibodies), or recessive Stargardt/cone-rod dystrophy cases.
NMNAT1 deletion in tumors may contribute to transformation by increasing ribosomal RNA synthesis.
mutations in nicotinamide nucleotide adenylyltransferase 1(NMNAT1) cause Leber congenital amaurosis
Mutations in NMNAT1 cause Leber congenital amaurosis with early-onset severe macular and optic atrophy.
NMNAT1 overexpression enhanced AMPK (show PRKAA1 Antibodies) activity in oxygen-glucose deprivation treated cortical neurons
An increased level of Nmnat protein in hiw mutants is both required and sufficient to inhibit axonal degeneration.
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.
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 adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death.
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.
nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons blocks axonal degeneration
Through NAMPT (show NAMPT Antibodies) activity, visfatin (show NAMPT Antibodies) contributes to vascular inflammation, causing atherothrombotic diseases linked to metabolic disorders.
demonstrated that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein; also demonstrated that SIRT1 (show SIRT1 Antibodies) is the downstream effector of increased Nmnat activity that leads to
Nmnat1 is significantly weaker than Wld(S) at protecting axons against traumatic or toxic injury in vitro, and has no detectable effect in vivo
This gene encodes an enzyme which catalyzes a key step in the biosynthesis of the coenzyme NAD. The encoded protein is one of several nicotinamide nucleotide adenylyltransferases. Studies in Drosophila and mammalian neurons have shown the encoded protein can confer protection to damaged neurons. This protection requires enzymatic activity which increases NAD levels and activates a nuclear deacetylase which is the protective molecule. Pseudogenes of this gene are located on chromosomes 1, 3, 4, 14 and 15.
nicotinamide mononucleotide adenylyltransferase 1
, Nicotinamide mononucleotide adenylyltransferase 1
, NMN adenylyltransferase 1
, NaMN adenylyltransferase 1
, nicotinate-nucleotide adenylyltransferase 1
, pyridine nucleotide adenylyltransferase 1
, naMN adenylyltransferase 1
, NAD(+) diphosphorylase
, NAD(+) pyrophosphorylase
, deamido-NAD(+) diphosphorylase
, deamido-NAD(+) pyrophosphorylase
, nicotinamide mononucleotide adenylyl transferase
, nicotinamide/nicotinate mononucleotide adenylyltransferase 1
, nicotinamide mononucleotide adenylyl transferase 1