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Zeng, Xing

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Zeng

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Xing

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Zeng, Xing

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2012 - 20192

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Author's Publications: search.filters.isAuthorOfPublication.c5b40f6b-5b02-429e-8aa2-a98753b5ddce

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    An APC/C inhibitor stabilizes cyclin B1 by prematurely terminating ubiquitination
    (2012) Zeng, Xing; King, Randall
    The Anaphase-Promoting Complex/Cyclosome (APC) is a ubiquitin ligase required for exit from mitosis. We previously showed that Tosyl Arginine Methyl Ester (TAME) inhibits APC-dependent proteolysis by competing with the C-terminal IR-tail of the APC activator Cdc20 for APC binding. Here we show that in the absence of APC substrates, TAME ejects Cdc20 from the APC by promoting Cdc20 auto-ubiquitination in its N-terminal region. Cyclin B1 antagonizes TAME's effect by promoting binding of free Cdc20 to the APC and suppressing Cdc20 auto-ubiquitination. Nevertheless, TAME stabilizes cyclin B1 in Xenopus extract by two mechanisms. First, it reduces the \(k_{cat}\) of the \(APC^{Cdc20}\)/cyclin B1 complex without affecting the \(K_m\), slowing the initial ubiquitination of unmodified cyclin B1. Second, as cyclin B1 becomes ubiquitinated, it loses its ability to promote Cdc20 binding to the APC in the presence of TAME. As a result, cyclin B1 ubiquitination terminates before reaching the threshold necessary for proteolysis.
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    Innervation of Thermogenic Adipose Tissue via a Calsyntenin 3β–S100b Axis
    (Springer Science and Business Media LLC, 2019-05) Zeng, Xing; Ye, Mengchen; Resch, Jon; Jedrychowski, Mark; Hu, Bo; Lowell, Bradford; Ginty, David; Spiegelman, Bruce
    The sympathetic nervous system drives brown and beige adipocyte thermogenesis via release of norepinephrine from local axons. However, the molecular basis underlying the higher levels of sympathetic innervation of thermogenic fat, compared to white fat, has remained elusive. Here we show that thermogenic adipocytes express a previously unknown, mammal-specific endoplasmic reticulum membrane protein, termed Calsyntenin-3β. Genetic loss or gain of Calsyntenin-3β in adipocytes reduces or enhances functional sympathetic innervation in adipose tissue respectively; Calsyntenin-3β ablation predisposes mice to obesity on a high fat diet. Mechanistically, Calsyntenin-3β promotes endoplasmic reticulum localization and secretion from brown adipocytes of S100b, a protein lacking a signal peptide. S100b stimulates neurite outgrowth from sympathetic neurons in vitro. S100b deficiency phenocopies Calsyntenin-3β deficiency, whereas forced expression of S100b in brown adipocytes rescues defective sympathetic innervation caused by Calsyntenin-3β ablation. Taken together, our data elucidate a mammal-specific mechanism of communication between thermogenic adipocytes and sympathetic neurons.