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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 (34) and NMNAT2 Proteins (18) and many more products for this protein.
Data indicate a chaperone function of nicotinamide mononucleotide adenylyl transferase (show NMNAT1 ELISA Kits) 2 (NMNAT2), independent from its enzymatic activity, and NMNAT2 complexes with heat shock protein 90 (HSP90 (show HSP90 ELISA Kits)) to refold aggregated protein substrates.
We confirmed association at NMNAT2 and identified independent SMG7 association with systemic lupus erythematosus in European American and Amerindian/Hispanic ancestries.
NMNAT2 might participate in tumorigenesis of CRC (show CALR ELISA Kits).
Knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53 (show TP53 ELISA Kits)-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53 (show TP53 ELISA Kits)-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 activity
Decreased endogenous NMNAT2 function caused by reduced CREB (show CREB1 ELISA Kits) 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 ELISA Kits) peripherally attached to membranes via palmitoylation and suggest that Nmnat2 is transported to synaptic terminals via an endosomal pathway.
Consistent with Skp1a (show SKP1 ELISA Kits) functioning through regulation of Nmnat2, Skp1a (show SKP1 ELISA Kits) knockdown fails to protect axons from Nmnat2 knockdown.
Active nerve degeneration requires SARM1 and MAP kinases, including DLK (show DAPK3 ELISA Kits), 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 dependent
Data indicate that thioesterases APT1 (show FAS ELISA Kits)/APT2 (show TAP2 ELISA Kits) depalmitoylate nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) and zDHHC17 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