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Size-Controlled Self-Assembly of Superparamagnetic Polymersomes
Hickey, Robert J.,Koski, Jason,Meng, Xin,Riggleman, Robert A.,Zhang, Peijun,Park, So-Jung American Chemical Society 2014 ACS NANO Vol.8 No.1
<P>We report the size-controlled self-assembly of polymersomes through the cooperative self-assembly of nanoparticles and amphiphilic polymers. Polymersomes densely packed with magnetic nanoparticles in the polymersome membrane (magneto-polymersome) were fabricated with a series of different sized iron oxide nanoparticles. The distribution of nanoparticles in a polymersome membrane was size-dependent; while small nanoparticles were dispersed in a polymer bilayer, large particles formed a well-ordered superstructure at the interface between the inner and outer layer of a bilayer membrane. The yield of magneto-polymersomes increased with increasing the diameter of incorporated nanoparticles. Moreover, the size of the polymersomes was effectively controlled by varying the size of incorporated nanoparticles. This size-dependent self-assembly was attributed to the polymer chain entropy effect and the size-dependent localization of nanoparticles in polymersome bilayers. The transverse relaxation rates (<I>r</I><SUB>2</SUB>) of magneto-polymersomes increased with increasing the nanoparticle diameter and decreasing the size of polymersomes, reaching 555 ± 24 s<SUP>–1</SUP> mM<SUP>–1</SUP> for 241 ± 16 nm polymersomes, which is the highest value reported to date for superparamagnetic iron oxide nanoparticles.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/ancac3/2014/ancac3.2014.8.issue-1/nn405012h/production/images/medium/nn-2013-05012h_0007.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/nn405012h'>ACS Electronic Supporting Info</A></P>
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WDR11‐mediated Hedgehog signalling defects underlie a new ciliopathy related to Kallmann syndrome
Kim, Yeon‐,Joo,Osborn, Daniel PS,Lee, Ji‐,Young,Araki, Masatake,Araki, Kimi,Mohun, Timothy,Kä,nsä,koski, Johanna,Brandstack, Nina,Kim, Hyun‐,Taek,Miralles, Francesc,Kim, Cheo John Wiley and Sons Inc. 2018 EMBO reports Vol.19 No.2
<P><B>Abstract</B></P><P>WDR11 has been implicated in congenital hypogonadotropic hypogonadism (CHH) and Kallmann syndrome (KS), human developmental genetic disorders defined by delayed puberty and infertility. However, WDR11's role in development is poorly understood. Here, we report that WDR11 modulates the Hedgehog (Hh) signalling pathway and is essential for ciliogenesis. Disruption of WDR11 expression in mouse and zebrafish results in phenotypic characteristics associated with defective Hh signalling, accompanied by dysgenesis of ciliated tissues. <I>Wdr11</I>‐null mice also exhibit early‐onset obesity. We find that WDR11 shuttles from the cilium to the nucleus in response to Hh signalling. WDR11 regulates the proteolytic processing of GLI3 and cooperates with the transcription factor EMX1 in the induction of downstream Hh pathway gene expression and gonadotrophin‐releasing hormone production. The CHH/KS‐associated human mutations result in loss of function of WDR11. Treatment with the Hh agonist purmorphamine partially rescues the WDR11 haploinsufficiency phenotypes. Our study reveals a novel class of ciliopathy caused by WDR11 mutations and suggests that CHH/KS may be a part of the human ciliopathy spectrum.</P>
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