Study summary · research use only
Apollon/Bruce is upregulated by Humanin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study, the authors report that Humanin, a short bioactive peptide, upregulates Apollon/Bruce. The abstract describes that Humanin inhibits several cell deaths via binding to its heterotrimeric Humanin receptor (htHNR), activating the JAK2/STAT3 pathway and increasing SH3BP5 expression. It reports that the htHNR/JAKs/STAT3 pathway increased mRNA and protein levels of Apollon/Bruce, an inhibitor-of-apoptosis protein, and that overexpression of Apollon/Bruce inhibited neuronal death caused by a London-type familial Alzheimer's-linked mutant (V642I) of amyloid beta precursor protein. The authors conclude Apollon/Bruce is upregulated by Humanin and could be a context-dependent effector.
Abstract
Humanin, a short bioactive peptide, inhibits a variety of cell deaths. Humanin-mediated inhibition of neuronal cell death, caused by an Alzheimer's disease (AD)-linked mutant gene occurs via binding of Humanin to its heterotrimeric Humanin receptor (htHNR), which results in the activation of the Janus-associated kinases (JAKs) and signal transducer and activator and transcription 3 (STAT3) signaling pathway. A previous study demonstrated that the Humanin-induced activation of the htHNR/JAK2/STAT3 signaling pathway leads to increased expression of SH3 domain-binding protein 5 (SH3BP5), which is an essential effector of Humanin's anti-cell death activity in some cultured neuronal cells. However, it remains unknown whether SH3BP5 is the sole effector of the Humanin signaling pathway via htHNR/JAKs/STAT3. Here we show that the Humanin signaling pathway via htHNR/JAKs/STAT3 increased the expression levels of mRNA and protein of Apollon/Bruce, an unusual member of the inhibitors of apoptosis proteins, and that overexpression of Apollon/Bruce inhibits neuronal death, caused by a London-type familial AD-linked mutant (V642I) of amyloid β precursor protein. Overall, the results indicate that expression of Apollon/Bruce is upregulated by Humanin, and Apollon/Bruce could be an effector of Humanin in a context-dependent manner.
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