ArticleJournal of molecular neuroscience : MN2005
Humanin attenuates apoptosis induced by DRPLA proteins with expanded polyglutamine stretches.
Article in Journal of molecular neuroscience : MN, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Single cell transcriptome analysis of the THY-Tau22 mouse model of Alzheimer's disease reveals sex-dependent dysregulations.Cell death discovery · 2024Article
- The Molecular Structure and Role of Humanin in Neural and Skeletal Diseases, and in Tissue Regeneration.Frontiers in cell and developmental biology · 2022Review
- The IL-27 component EBI-3 and its receptor subunit IL-27Rα are essential for the cytoprotective action of humanin on male germ cells†.Biology of reproduction · 2021Article
- The humanin peptide mediates ELP nanoassembly and protects human retinal pigment epithelial cells from oxidative stress.Nanomedicine : nanotechnology, biology, and medicine · 2020Article
- Humanin Does Not Protect Against STZ-Induced Spatial Memory Impairment.Journal of molecular neuroscience : MN · 2015Article
- Humanin protects against chemotherapy-induced stage-specific male germ cell apoptosis in rats.Andrology · 2015Article
- Protective effects of Humanin and calmodulin-like skin protein in Alzheimer's disease and broad range of abnormalities.Molecular neurobiology · 2015Review
- Apoptosis in Alzheimer's disease: an understanding of the physiology, pathology and therapeutic avenues.Neurochemical research · 2014Review
- The cytoprotective peptide humanin is induced and neutralizes Bax after pro-apoptotic stress in the rat testis.Andrology · 2013Article
- Humanin: a harbinger of mitochondrial-derived peptides?Trends in endocrinology and metabolism: TEM · 2013Article
- The emerging role of the mitochondrial-derived peptide humanin in stress resistance.Journal of molecular endocrinology · 2013Review
- A humanin derivative reduces amyloid beta accumulation and ameliorates memory deficit in triple transgenic mice.PloS one · 2011Article
- Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Journal of genetics · 2010Review
- Humanin and the receptors for humanin.Molecular neurobiology · 2010Review
- Structural and functional characterization of the human protein kinase ASK1.Structure (London, England : 1993) · 2007Article
- Neuroprotection against neurodegenerative diseases: development of a novel hybrid neuroprotective peptide Colivelin.Molecular neurobiology · 2007Review
- Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dentatorubral-pallidoluysian atrophy (DRPLA) is an autosomal-dominant neurodegenerative disorder caused by expansion of CAG repeats in the DRPLA gene, which codes for a polyglutamine (polyQ) stretch. The expanded polyQs are known to form intracellular aggregates and to confer neurotoxic activity. Recent studies have indicated that activation of apoptosis signal-regulating kinase 1 (ASK1) is involved in polyQ-induced apoptosis. Humanin (HN) is an endogenous peptide that inhibits neuronal cell death caused by mutant Alzheimer's disease genes, and this neuroprotective factor has recently been reported to suppress apoptosis by inhibiting activation of ASK1. To test the anti-ASK1 effect of HN on polyQ neurotoxicity, we constructed neuronal PC12 cells expressing expanded polyQs under the control of the Tet-Off system. Using this cell line, we showed that HN suppresses apoptotic cell death induced by expanded polyQs. However, the suppression was incomplete, suggesting that polyQs also stimulate other pathogenic cascades unrelated to ASK1. We further showed that HN suppresses polyQ aggregate formation. This result implied the possibility that aggregation is also related to the polyQ-mediated cascade involving ASK1 activation. Although the details remain uncertain, our results suggest that ASK1 is potentially involved in pathogenesis of DRPLA and that HN might contribute partially to the suppression of neurodegeneration in polyQ diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.