Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Accumulation of labile zinc in neurons and astrocytes in the spinal cords of G93A SOD-1 transgenic mice.

Neurobiology of disease - 1 May 2009

Kim Jean, Kim Tae-Youn, Hwang Jung Jin, Lee Joo-Yong, Shin Jin-Hee, Gwag Byung Joo, Koh Jae-Young

Abstract excerpt

Zinc dyshomeostasis may trigger oxidative stress, which is likely the key mechanism of neuronal death in amyotrophic lateral sclerosis (ALS), including familial forms such as G93A SOD-1 ALS. Since zinc binding by G93A SOD-1 is weaker than by normal SOD-1, we assessed whether labile zinc levels are altered in the spinal cords of G93A SOD-1 transgenic (Tg) mice. Whereas no zinc-containing cells were found in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aldehydes
Share to Astrocytes
Share to Chelating Agents

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Motor Neurons

Share to Nerve Degeneration

Share to Spinal Cord

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 19344646
DOI: 10.1016/j.nbd.2009.01.004

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Accumulation of labile zinc in neurons and astrocytes in the spinal cords of G93A SOD-1 transgenic mice.PMID 19344646Read ↗

Glia and zinc in ageing and Alzheimerâ€™s disease: a mechanism for cognitive decline?Semantic proximity Read ↗

The Metallothionein/Thionein System: An Oxidoreductive Metabolic Zinc LinkSemantic proximity Read ↗

Zinc in the spinal cord of a mutant SOD1 mouse model of ALS.Semantic proximity Read ↗

Disease progression in a transgenic model of familial amyotrophic lateral sclerosis is dependent on both neuronal and non-neuronal zinc binding proteins.Semantic proximity Read ↗

Overexpression of metallothionein protects cultured motor neurons against oxidative stress, but not mutant Cu/Zn-superoxide dismutase toxicity.Semantic proximity Read ↗

Zinc deficiency impairs functional recovery after spinal cord injury by promoting NF-κB activity in macrophagesSemantic proximity Read ↗

Metallothionein proteins expression, copper and zinc concentrations, and lipid peroxidation level in a rodent model for amyotrophic lateral sclerosis.Semantic proximity Read ↗

Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem CellsSemantic proximity Read ↗

Decreased zinc affinity of amyotrophic lateral sclerosis-associated superoxide dismutase mutants leads to enhanced catalysis of tyrosine nitration by peroxynitrite.Semantic proximity Read ↗

Polyphenols Suppress Intracellular Zinc Deficiency–Induced ROS Production and NLRP3 Inflammasome Activation in Microglia and Neuronal CellsSemantic proximity Read ↗

Neurometals in the Pathogenesis of Prion DiseasesSemantic proximity Read ↗

Induction of nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide dismutase.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.