{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T18:48:43Z","timestamp":1793386123789,"version":"4.5.0"},"reference-count":43,"publisher":"American Society for Cell Biology (ASCB)","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MBoC"],"published-print":{"date-parts":[[2009,6,15]]},"abstract":"<jats:p>Humanin (HN) inhibits neuronal death induced by various Alzheimer's disease (AD)-related insults via an unknown receptor on cell membranes. Our earlier study indicated that the activation of STAT3 was essential for HN-induced neuroprotection, suggesting that the HN receptor may belong to the cytokine receptor family. In this study, a series of loss-of-function tests indicated that gp130, the common subunit of receptors belonging to the IL-6 receptor family, was essential for HN-induced neuroprotection. Overexpression of ciliary neurotrophic factor receptor \u03b1 (CNTFR) and\/or the IL-27 receptor subunit, WSX-1, but not that of any other tested gp130-related receptor subunit, up-regulated HN binding to neuronal cells, whereas siRNA-mediated knockdown of endogenous CNTFR and\/or WSX-1 reduced it. These results suggest that both CNTFR and WSX-1 may be also involved in HN binding to cells. Consistent with these results, loss-of-functions of CNTFR or WSX-1 in neuronal cells nullified their responsiveness to HN-mediated protection. In vitro\u2013reconstituted binding assays showed that HN, but not the other control peptide, induced the hetero-oligomerization of CNTFR, WSX-1, and gp130. Together, these results indicate that HN protects neurons by binding to a complex or complexes involving CNTFR\/WSX-1\/gp130.<\/jats:p>","DOI":"10.1091\/mbc.e09-02-0168","type":"journal-article","created":{"date-parts":[[2009,4,22]],"date-time":"2009-04-22T20:44:56Z","timestamp":1240433096000},"page":"2864-2873","source":"Crossref","is-referenced-by-count":187,"title":["Humanin Inhibits Neuronal Cell Death by Interacting with a Cytokine Receptor Complex or Complexes Involving CNTF Receptor \u03b1\/WSX-1\/gp130"],"prefix":"10.1091","volume":"20","author":[{"given":"Yuichi","family":"Hashimoto","sequence":"first","affiliation":[{"name":"*Department of Pharmacology and Neuroscience, Tokyo Medical University, Shinjuku-ku, Tokyo 160-8402, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megumi","family":"Kurita","sequence":"additional","affiliation":[{"name":"*Department of Pharmacology and Neuroscience, Tokyo Medical University, Shinjuku-ku, Tokyo 160-8402, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sadakazu","family":"Aiso","sequence":"additional","affiliation":[{"name":"Departments of \u2020Anatomy, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ikuo","family":"Nishimoto","sequence":"additional","affiliation":[{"name":"Pharmacology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaaki","family":"Matsuoka","sequence":"additional","affiliation":[{"name":"*Department of Pharmacology and Neuroscience, Tokyo Medical University, Shinjuku-ku, Tokyo 160-8402, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1076","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"152","DOI":"10.1016\/j.bbrc.2005.01.100","volume":"329","author":"Benaki D.","year":"2005","journal-title":"Biochem. 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