NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. - Wikidata - wikimedia - TriplyDB

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration.

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration.

http://www.wikidata.org/entity/Q34518882

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Drosophila NMNAT maintains neural integrity independent of its NAD synthesis activity Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons Enzymes in the NAD+ salvage pathway regulate SIRT1 activity at target gene promoters Mutations in NMNAT1 cause Leber congenital amaurosis and identify a new disease pathway for retinal degeneration Protective effects and mechanisms of sirtuins in the nervous system Wallerian degeneration: the innate-immune response to traumatic nerve injury Activation of SIRT3 by the NAD⁺ precursor nicotinamide riboside protects from noise-induced hearing loss Mislocalization of neuronal mitochondria reveals regulation of Wallerian degeneration and NMNAT/WLD(S)-mediated axon protection independent of axonal mitochondria.Mammalian sirtuins: biological insights and disease relevance Death Receptor 6 Promotes Wallerian Degeneration in Peripheral Axons.Wallerian-like degeneration of central neurons after synchronized and geometrically registered mass axotomy in a three-compartmental microfluidic chip Deletions within its subcellular targeting domain enhance the axon protective capacity of Nmnat2 in vivo A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration Novel compound heterozygous NMNAT1 variants associated with Leber congenital amaurosis.The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways.Isoform-specific targeting and interaction domains in human nicotinamide mononucleotide adenylyltransferases Nicotinamide adenine dinucleotide metabolism as an attractive target for drug discovery.Wallerian degeneration, wld(s), and nmnat.Synaptic protection in the brain of WldS mice occurs independently of age but is sensitive to gene-dose.Preserve and protect: maintaining axons within functional circuits.Targeting anti-inflammatory treatment can ameliorate injury-induced neuropathic pain.Reducing expression of NAD+ synthesizing enzyme NMNAT1 does not affect the rate of Wallerian degeneration.NAD synthase NMNAT acts as a chaperone to protect against neurodegeneration.Subcellular localization determines the stability and axon protective capacity of axon survival factor Nmnat2.Nicotinamide mononucleotide adenylyl transferase-mediated axonal protection requires enzymatic activity but not increased levels of neuronal nicotinamide adenine dinucleotide Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death.Chemical genetic-mediated spatial regulation of protein expression in neurons reveals an axonal function for wld(s).WldS but not Nmnat1 protects dopaminergic neurites from MPP+ neurotoxicity.Impact of Genetic Reduction of NMNAT2 on Chemotherapy-Induced Losses in Cell Viability In Vitro and Peripheral Neuropathy In Vivo Differential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene.Protection of mouse retinal ganglion cell axons and soma from glaucomatous and ischemic injury by cytoplasmic overexpression of Nmnat1.Mitochondrial dysfunction induced by heat stress in cultured rat CNS neurons.UBE4B: a promising regulatory molecule in neuronal death and survival.Molecular chaperones protect against JNK- and Nmnat-regulated axon degeneration in Drosophila Modified cell cycle status in a mouse model of altered neuronal vulnerability (slow Wallerian degeneration; Wlds).Wld S requires Nmnat1 enzymatic activity and N16-VCP interactions to suppress Wallerian degeneration.Wld S protein requires Nmnat activity and a short N-terminal sequence to protect axons in mice Nmnat delays axonal degeneration caused by mitochondrial and oxidative stress The purine nucleosides adenosine and guanosine delay axonal degeneration in vitro Transgenic mice expressing the Nmnat1 protein manifest robust delay in axonal degeneration in vivo.

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NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration.

http://www.wikidata.org/entity/Q34518882

description

2006 nî lūn-bûn

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2006 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2006 թվականի ապրիլին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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type

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NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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prefLabel

NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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NAD(+) and axon degeneration r ...... delay Wallerian degeneration.

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A Silva

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B Beirowski

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G Fang

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1

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