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

Nuclear translocation of AMPK-alpha1 potentiates striatal neurodegeneration in Huntington's disease.

The Journal of cell biology - 25 Jul 2011

Ju Tz-Chuen, Chen Hui-Mei, Lin Jiun-Tsai, Chang Ching-Pang, Chang Wei-Cheng, Kang Jheng-Jie, Sun Cheng-Pu, Tao Mi-Hua, Tu Pang-Hsien, Chang Chen, Dickson Dennis W, Chern Yijuang

Abstract excerpt

Adenosine monophosphate-activated protein kinase (AMPK) is a major energy sensor that maintains cellular energy homeostasis. Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of CAG repeats in the huntingtin (Htt) gene. In this paper, we report that activation of the α1 isoform of AMPK (AMPK-α1) occurred in striatal neurons of humans and mice with HD. Overactivation of AMPK in the...

Read the complete abstract on PubMed

Topics

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

Share to Active Transport, Cell Nucleus
Share to AMP-Activated Protein Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calcium-Calmodulin-Dependent Protein Kinase Type 2

Share to Huntingtin Protein

Share to Huntington Disease

Share to Neostriatum

Share to Nerve Degeneration

Share to Proto-Oncogene Proteins c-bcl-2

Source

Open in PubMed Open full text

Identifiers

PMID: 21768291
DOI: 10.1083/jcb.201105010
PMCID: PMC3144412

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Nuclear translocation of AMPK-alpha1 potentiates striatal neurodegeneration in Huntington's disease.PMID 21768291Read ↗

AMPK activation protects from neuronal dysfunction and vulnerability across nematode, cellular and mouse models of Huntington's disease.Semantic proximity Read ↗

Conditional disruption of AMP kinase in dopaminergic neurons promotes Parkinson’s disease-associated phenotypes in miceSemantic proximity Read ↗

Modulating the catalytic activity of AMPK has neuroprotective effects against α-synuclein toxicity.Semantic proximity Read ↗

Energy dysfunction in Huntington’s disease: insights from PGC-1α, AMPK, and CKBSemantic proximity Read ↗

Conditional disruption of AMP kinase in dopaminergic neurons promotes Parkinson's disease-associated phenotypes in vivo.Semantic proximity Read ↗

Contribution of Energy Dysfunction to Impaired Protein Translation in Neurodegenerative DiseasesSemantic proximity Read ↗

SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice.Semantic proximity Read ↗

GLP-1 Analogue Liraglutide Attenuates Mutant Huntingtin-Induced Neurotoxicity by Restoration of Neuronal Insulin SignalingSemantic proximity Read ↗

Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathwaySemantic proximity Read ↗

Targeting energy metabolism in Huntington's disease.Semantic proximity Read ↗

PGC-1α rescues Huntington's disease proteotoxicity by preventing oxidative stress and promoting TFEB function.Semantic proximity Read ↗

Activation of AMP-activated protein kinase in cerebella of Atm-/- mice is attributable to accumulation of reactive oxygen species.Semantic proximity Read ↗

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