Humanin: After the discovery

Takako Niikura; Tomohiro Chiba; Sadakazu Aiso; Masaaki Matsuoka; Ikuo Nishimoto

doi:10.1385/MN:30:3:327

Humanin: After the discovery

Takako Niikura, Tomohiro Chiba, Sadakazu Aiso, Masaaki Matsuoka, Ikuo Nishimoto

Research output: Contribution to journal › Review article › peer-review

38 Citations (Scopus)

Abstract

Humanin (HN) is a novel neuroprotective factor that consists of 24 amino acid residues. HN suppresses neuronal cell death caused by Alzheimer's disease (AD)-specific insults, including both amyloid-β (βAβ) peptides and familial AD-causative genes. Cerebrovascular smooth muscle cells are also protected from Aβ toxicity by HN, suggesting that HN affects both neuronal and non-neuronal cells when they are exposed to AD-related cytotoxicity. HN peptide exerts a neuroprotective effect through the cell surface via putative receptor(s). HN activates a cellular signaling cascade that intervenes (at least) in activation of c-Jun N-terminal kinase. The highly selective effect of HN on AD-relevant cell death indicates that HN is promising for AD therapy. Additionally, a recent study showed that intracellularly overexpressed HN suppressed mitochondriamediated apoptosis by inhibiting Bax activity.

Original language	English
Pages (from-to)	327-340
Number of pages	14
Journal	Molecular Neurobiology
Volume	30
Issue number	3
DOIs	https://doi.org/10.1385/MN:30:3:327
Publication status	Published - 2004 Dec
Externally published	Yes

Keywords

Alzheimer's disease
Amyloid β
AβPP
Cell death
Humanin
Neuroprotection

ASJC Scopus subject areas

Neurology
Cellular and Molecular Neuroscience

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title = "Humanin: After the discovery",

abstract = "Humanin (HN) is a novel neuroprotective factor that consists of 24 amino acid residues. HN suppresses neuronal cell death caused by Alzheimer's disease (AD)-specific insults, including both amyloid-β (βAβ) peptides and familial AD-causative genes. Cerebrovascular smooth muscle cells are also protected from Aβ toxicity by HN, suggesting that HN affects both neuronal and non-neuronal cells when they are exposed to AD-related cytotoxicity. HN peptide exerts a neuroprotective effect through the cell surface via putative receptor(s). HN activates a cellular signaling cascade that intervenes (at least) in activation of c-Jun N-terminal kinase. The highly selective effect of HN on AD-relevant cell death indicates that HN is promising for AD therapy. Additionally, a recent study showed that intracellularly overexpressed HN suppressed mitochondriamediated apoptosis by inhibiting Bax activity.",

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author = "Takako Niikura and Tomohiro Chiba and Sadakazu Aiso and Masaaki Matsuoka and Ikuo Nishimoto",

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T2 - After the discovery

AU - Niikura, Takako

AU - Chiba, Tomohiro

AU - Aiso, Sadakazu

AU - Matsuoka, Masaaki

AU - Nishimoto, Ikuo

PY - 2004/12

Y1 - 2004/12

N2 - Humanin (HN) is a novel neuroprotective factor that consists of 24 amino acid residues. HN suppresses neuronal cell death caused by Alzheimer's disease (AD)-specific insults, including both amyloid-β (βAβ) peptides and familial AD-causative genes. Cerebrovascular smooth muscle cells are also protected from Aβ toxicity by HN, suggesting that HN affects both neuronal and non-neuronal cells when they are exposed to AD-related cytotoxicity. HN peptide exerts a neuroprotective effect through the cell surface via putative receptor(s). HN activates a cellular signaling cascade that intervenes (at least) in activation of c-Jun N-terminal kinase. The highly selective effect of HN on AD-relevant cell death indicates that HN is promising for AD therapy. Additionally, a recent study showed that intracellularly overexpressed HN suppressed mitochondriamediated apoptosis by inhibiting Bax activity.

AB - Humanin (HN) is a novel neuroprotective factor that consists of 24 amino acid residues. HN suppresses neuronal cell death caused by Alzheimer's disease (AD)-specific insults, including both amyloid-β (βAβ) peptides and familial AD-causative genes. Cerebrovascular smooth muscle cells are also protected from Aβ toxicity by HN, suggesting that HN affects both neuronal and non-neuronal cells when they are exposed to AD-related cytotoxicity. HN peptide exerts a neuroprotective effect through the cell surface via putative receptor(s). HN activates a cellular signaling cascade that intervenes (at least) in activation of c-Jun N-terminal kinase. The highly selective effect of HN on AD-relevant cell death indicates that HN is promising for AD therapy. Additionally, a recent study showed that intracellularly overexpressed HN suppressed mitochondriamediated apoptosis by inhibiting Bax activity.

KW - Alzheimer's disease

KW - Amyloid β

KW - AβPP

KW - Cell death

KW - Humanin

KW - Neuroprotection

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JO - Molecular Neurobiology

JF - Molecular Neurobiology

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ER -

Humanin: After the discovery

Abstract

Keywords

ASJC Scopus subject areas

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