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NMNAT2 product belongs to the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme family, members of which catalyze an essential step in NAD (NADP) biosynthetic pathway. Additionally we are shipping NMNAT2 Antibodies (36) and many more products for this protein.
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Knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53 (show TP53 Proteins)-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53 (show TP53 Proteins)-mediated signaling.
Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is essential for axon growth and survival.
Overexpression of NMNAT2 in colorectal cancer cells renders them sensitive to Tiazofurin antineoplastic action.
affects tau phosphorylation by regulating PP2A (show PPP2R4 Proteins) activity
Decreased endogenous NMNAT2 function caused by reduced CREB (show CREB1 Proteins) signaling during pathological insults may be one of underlying mechanisms for neuronal death in tauopathies
that overexpression of Nmnat2 in M-cells significantly delayed axon degeneration in vivo
Nmnat2 is a neuronal protein (show LRCH1 Proteins) peripherally attached to membranes via palmitoylation and suggest that Nmnat2 is transported to synaptic terminals via an endosomal pathway.
NMNAT1 (show NMNAT1 Proteins) is a nuclear protein (show RDBP Proteins), whereas NMNAT2 and -3 are localized to the Golgi complex and the mitochondria
ATP binds before NMN (show NTS Proteins) with Golgi apparatus NMNAT2. NMNH conversion to NADH by NMNAT1 (show NMNAT1 Proteins) and NMNAT3 (show NMNAT3 Proteins) occurs at similar rates, conversion by NMNAT2 is much slower.
Active nerve degeneration requires SARM1 (show SARM1 Proteins) and MAP kinases, including DLK (show DAPK3 Proteins), while the NAD+ synthetic enzyme NMNAT2 prevents degeneration.
nicotinamide mononucleotide adenylyltransferase 2-depletion-dependent degeneration of established axons and restricted extension of developing axons are thus both SARM1 (show SARM1 Proteins) dependent
Data indicate that thioesterases APT1 (show FAS Proteins)/APT2 (show TAP2 Proteins) depalmitoylate nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) and zDHHC17 (show ZDHHC17 Proteins) is the strongest candidate palmitoyltransferase for NMNAT2.
Complete loss of Nmnat2 leads to a mature but distended bladder in utero and is not compatible with survival. Moderate loss of Nmnat2 has no effect on bladder development, survival, and has only modest effects on bladder function later in life.
Together, our results establish Nmnat2 localisation and turnover as a valuable target for modulating axon degeneration in vivo.
results suggest an essential role for NMNAT2 during axon growth
Nmnat2 activity supports axon survival through a site of action distinct from Nmnat2 transport vesicles.
Nmnat2 is involved in axon development or survival in a mammal.
This gene product belongs to the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme family, members of which catalyze an essential step in NAD (NADP) biosynthetic pathway. Unlike the other human family member, which is localized to the nucleus, and is ubiquitously expressed\; this enzyme is cytoplasmic, and is predominantly expressed in the brain. Two transcript variants encoding different isoforms have been found for this gene.
NMN adenylyltransferase 2
, naMN adenylyltransferase 1
, nicotinamide mononucleotide adenylyltransferase 2
, nicotinate-nucleotide adenylyltransferase 1
, nicotinamide nucleotide adenylyltransferase 2
, NaMN adenylyltransferase 2
, nicotinate-nucleotide adenylyltransferase 2
, pyridine nucleotide adenylyltransferase 2