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

Neuronal over-expression of chromogranin A accelerates disease onset in a mouse model of ALS.

Journal of neurochemistry - 1 Dec 2010

Ezzi Samer Abou, Larivière Roxanne, Urushitani Makoto, Julien Jean-Pierre

Abstract excerpt

Recent studies provided evidence that chromogranins can interact with mutant superoxide dismutase 1 (SOD1) and that chromogranin B (CgB) may act as a susceptibility gene and modifier of onset in amyotrophic lateral sclerosis (ALS). To further investigate the role of chromogranins in ALS pathogenesis, we generated SOD1(G37R) mice that over-express CgA under the control of Thy1 promoter. Here, we report that...

Read the complete abstract on PubMed

Topics

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

Share to Chromogranin A
Share to Glial Fibrillary Acidic Protein

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Immunoprecipitation

Share to Motor Neurons

Share to Nerve Degeneration

Share to Neuromuscular Junction

Share to Spinal Cord

Share to Thy-1 Antigens

Source

Identifiers

PMID: 20807312
DOI: 10.1111/j.1471-4159.2010.06979.x

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Neuronal over-expression of chromogranin A accelerates disease onset in a mouse model of ALS.PMID 20807312Read ↗

Chromogranin-mediated secretion of mutant superoxide dismutase proteins linked to amyotrophic lateral sclerosis.Semantic proximity Read ↗

[Implications of successful immunotherapy in ALS model mice].Semantic proximity Read ↗

Mechanisms of disease: motoneuron disease aggravated by transgenic expression of a functionally modified AMPA receptor subunit.Semantic proximity Read ↗

Sex-dependent effects of chromogranin B P413L allelic variant as disease modifier in amyotrophic lateral sclerosis.Semantic proximity Read ↗

Endocannabinoids accumulate in spinal cord of SOD1<sup>G93A</sup> transgenic miceSemantic proximity Read ↗

Chromogranin B P413L variant as risk factor and modifier of disease onset for amyotrophic lateral sclerosis.Semantic proximity Read ↗

Pre-symptomatic alterations in subcellular betaCGRP distribution in motor neurons precede astrogliosis in ALS mice.Semantic proximity Read ↗

Possible role of autoantibodies in the pathophysiology of GM2 gangliosidosesSemantic proximity Read ↗

Chromogranin A (CgA) Deficiency Attenuates Tauopathy by Altering Epinephrine–Alpha-Adrenergic Receptor SignalingSemantic proximity Read ↗

Possible role of autoantibodies in the pathophysiology of GM2 gangliosidosesSemantic proximity Read ↗

A dynein mutation attenuates motor neuron degeneration in SOD1(G93A) mice.Semantic proximity Read ↗

Chromogranins A and B are key proteins in amine accumulation, but the catecholamine secretory pathway is conserved without them.Semantic proximity Read ↗

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