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NAT8L encodes a single-pass membrane protein, which contains a conserved sequence of the GCN5 or NAT superfamily of N-acetyltransferases and is a member of the N-acyltransferase (NAT) superfamily. De plus, nous expédions N-Acetyltransferase 8-Like (GCN5-Related, Putative) Anticorps (23) et N-Acetyltransferase 8-Like (GCN5-Related, Putative) Kits (18) et beaucoup plus de produits pour cette protéine.
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The findings of this study indicated that the striatal expression of N-acetylaspartate synthetase Shati/Nat8l plays a role in major depressive disorder via the metabotropic glutamate receptor 3-mediated functional control of the serotonergic neuronal system.
Results showed that the Shati/Nat8L mRNA was increased by methamphetamine-induced CREB pathway via dopamine D1 receptor signaling in mouse nucleus accumbens. These findings may contribute to development of a clinical tool for methamphetamine addiction.
Results showed that both Shati+/- and Shati-/- mice demonstrated lower levels of NAA in the brain than Shati+/+ mice, suggesting that SHATI predominantly regulates NAA content in the brain
Study shows that Shati/Nat8l in the neuron may induce axon outgrowth by ATP synthesis and not through mGluR3 signaling.
Dysregulated expression of Nat8L is associated with deficits in oxidative phosphorylation in 5xFAD model of Alzheimer disease.
results indicate that Shati/Nat8l in the Nucleus Accumbens, but not in the dorsal striatum, plays a suppressive role in the behavioral responses to METHamphetamine by controlling the dopaminergic system via activation of group II mGlutamate receptors
The results of this study showed that Deletion of NAT8L increases dopamine D1 receptor on the cell surface in the nucleus accumbens, accelerating methamphetamine dependence in mice.
Nat8l impacts on the brown adipogenic phenotype
Deficiency of SHATI may affect behavior.
shati expression affects emoutional behaivors in mice
Nat8l is highly specific to aspartate. It is localized in mitochondria and microsomes, with a pattern comparable to the localization of NAA in brain. It is similar to NAG synthetase in catalytic mechanism without the involvement of cysteine.
Results indicated that NAT8L, but not NAT14, catalysed the synthesis of NAA from L-aspartate and acetyl-CoA.
Roles of shati in methamphetamine (METH)-regulated behavioral alternations are likely to be mediated by its inhibitory effects on METH-induced increase of dopamine(DA) overflow in nucleus accumbens and METH-induced decrease in DA uptake in midbrain.
Nat8l CpG island methylation ratios were lower in the patients with schizophrenia than in the healthy controls.
Characterization and recombinant expression of the nat8l gene that codes for ANAT.
NAA is produced specifically in NSCLC tumors through NAT8L overexpression, and its extracellular secretion can be detected in blood
This study demonistrated that the human NAT8L gene related to reward dependence, a personality trait, and grey matter volume in the caudate nucleus in healthy subjects, suggesting that NAT8L might also affect human personality
The aim of the present study was to determine which regions of the protein are important for its catalytic activity and its subcellular localization.
This gene encodes a single-pass membrane protein, which contains a conserved sequence of the GCN5 or NAT superfamily of N-acetyltransferases and is a member of the N-acyltransferase (NAT) superfamily. This protein is a neuron-specific protein and is the N-acetylaspartate (NAA) biosynthetic enzyme, catalyzing the NAA synthesis from L-aspartate and acetyl-CoA. NAA is a major storage and transport form of acetyl coenzyme A specific to the nervous system. The gene mutation results in primary NAA deficiency (hypoacetylaspartia).
, N-acetylaspartate synthetase
, N-acetyltransferase 8-like protein
, NAA synthetase
, camello 3
, protein Shati
, camello-like protein 3