<?xml version="1.0" encoding="UTF-8"?>
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  <title>DSpace Collection:</title>
  <link rel="alternate" href="http://hdl.handle.net/2440/11253" />
  <subtitle />
  <id>http://hdl.handle.net/2440/11253</id>
  <updated>2013-06-19T16:24:20Z</updated>
  <dc:date>2013-06-19T16:24:20Z</dc:date>
  <entry>
    <title>Vitamin D actions to regulate calcium and skeletal homeostasis</title>
    <link rel="alternate" href="http://hdl.handle.net/2440/78123" />
    <author>
      <name>Anderson, Paul Hamill</name>
    </author>
    <author>
      <name>Turner, Andrew Grant</name>
    </author>
    <author>
      <name>Morris, Howard Arthur</name>
    </author>
    <id>http://hdl.handle.net/2440/78123</id>
    <updated>2013-05-31T06:30:32Z</updated>
    <published>2011-12-31T13:30:00Z</published>
    <summary type="text">Title: Vitamin D actions to regulate calcium and skeletal homeostasis
Author: Anderson, Paul Hamill; Turner, Andrew Grant; Morris, Howard Arthur</summary>
    <dc:date>2011-12-31T13:30:00Z</dc:date>
  </entry>
  <entry>
    <title>Solution structure and membrane interactions of the antimicrobial peptide Fallaxidin 4.1a: An NMR and QCM study</title>
    <link rel="alternate" href="http://hdl.handle.net/2440/57828" />
    <author>
      <name>Sherman, Patrick James</name>
    </author>
    <author>
      <name>Jackway, Rebecca Jo</name>
    </author>
    <author>
      <name>Gehman, John D.</name>
    </author>
    <author>
      <name>Praporski, Slavica</name>
    </author>
    <author>
      <name>McCubbin, George A.</name>
    </author>
    <author>
      <name>Mechler, Adam</name>
    </author>
    <author>
      <name>Martin, Lisandra L.</name>
    </author>
    <author>
      <name>Separovic, Frances</name>
    </author>
    <author>
      <name>Bowie, John Hamilton</name>
    </author>
    <id>http://hdl.handle.net/2440/57828</id>
    <updated>2010-04-22T09:31:23Z</updated>
    <published>2008-12-31T13:30:00Z</published>
    <summary type="text">Title: Solution structure and membrane interactions of the antimicrobial peptide Fallaxidin 4.1a: An NMR and QCM study
Author: Sherman, Patrick James; Jackway, Rebecca Jo; Gehman, John D.; Praporski, Slavica; McCubbin, George A.; Mechler, Adam; Martin, Lisandra L.; Separovic, Frances; Bowie, John Hamilton
Description: Copyright © 2009 American Chemical Society</summary>
    <dc:date>2008-12-31T13:30:00Z</dc:date>
  </entry>
  <entry>
    <title>The HIF1 alpha-inducible pro-cell death gene BNIP3 is a novel target of SIM2s repression through cross-talk on the hypoxia response element</title>
    <link rel="alternate" href="http://hdl.handle.net/2440/57698" />
    <author>
      <name>Farrall, Alexandra Louise</name>
    </author>
    <author>
      <name>Whitelaw, Murray Leslie</name>
    </author>
    <id>http://hdl.handle.net/2440/57698</id>
    <updated>2010-04-15T09:31:48Z</updated>
    <published>2008-12-31T13:30:00Z</published>
    <summary type="text">Title: The HIF1 alpha-inducible pro-cell death gene BNIP3 is a novel target of SIM2s repression through cross-talk on the hypoxia response element; The HIF1α-inducible pro-cell death gene BNIP3 is a novel target of SIM2s repression through cross-talk on the hypoxia response element
Author: Farrall, Alexandra Louise; Whitelaw, Murray Leslie
Abstract: The short isoform of single-minded 2 (SIM2s), a basic helix–loop–helix/PAS (bHLH/PAS) transcription factor, is upregulated in pancreatic and prostate tumours; however, a mechanistic role for SIM2s in these cancers is unknown. Microarray studies in prostate DU145 cells identified the pro-cell death gene, BNIP3 (Bcl-2/adenovirus E1B 19 kDa interacting protein 3), as a novel putative target of SIM2s repression. Further validation showed BNIP3 repression in several prostate and pancreatic carcinoma-derived cell lines with ectopic expression of human SIM2s. BNIP3 levels are enhanced in prostate carcinoma cells upon short interfering (si)RNA-mediated knockdown of endogenous SIM2s. Chromatin immunoprecipitation and promoter studies show that SIM2s represses BNIP3 through its activities at the proximal promoter hypoxia response element (HRE), the site through which the bHLH/PAS family member, hypoxia-inducible factor 1α (HIF1α), induces BNIP3. SIM2s attenuates BNIP3 hypoxic induction via the HRE, and increased hypoxic induction of BNIP3 occurs with siRNA knockdown of endogenous SIM2s in prostate PC3AR+ cells. BNIP3 is implicated in hypoxia-induced cell death processes. Prolonged treatment of PC3AR+ cells with hypoxia mimetics, DP and DMOG, confers hypoxia-induced autophagy, measured by enhanced LC3-II levels and SQSTM1/p62 turnover. We show that PC3AR+ cells expressing ectopic SIM2s have enhanced survival in these conditions. Induction of LC3-II and turnover of SQSTM1/p62 are attenuated in PC3AR+/SIM2s DMOG and hypoxia-treated cells, suggesting that SIM2s may attenuate autophagic cell death processes, perhaps through BNIP3 repression. These data show, for the first time, SIM2s cross-talk on an endogenous HRE. SIM2s' functional interference with HIF1α activities on BNIP3 may indicate a novel role for SIM2s in promoting tumourigenesis.
Description: © 2009 Macmillan Publishers Limited. All rights reserved</summary>
    <dc:date>2008-12-31T13:30:00Z</dc:date>
  </entry>
  <entry>
    <title>Why do phage play dice?</title>
    <link rel="alternate" href="http://hdl.handle.net/2440/56804" />
    <author>
      <name>Avlund, Mikkel</name>
    </author>
    <author>
      <name>Dodd, Ian Burwell</name>
    </author>
    <author>
      <name>Semsey, Szabolcs</name>
    </author>
    <author>
      <name>Sneppen, Kim</name>
    </author>
    <author>
      <name>Krishna, Sandeep</name>
    </author>
    <id>http://hdl.handle.net/2440/56804</id>
    <updated>2010-03-18T08:32:07Z</updated>
    <published>2008-12-31T13:30:00Z</published>
    <summary type="text">Title: Why do phage play dice?
Author: Avlund, Mikkel; Dodd, Ian Burwell; Semsey, Szabolcs; Sneppen, Kim; Krishna, Sandeep
Abstract: Phage lambda is among the simplest organisms that make a developmental decision. An infected bacterium goes either into the lytic state, where the phage particles rapidly replicate and eventually lyse the cell, or into a lysogenic state, where the phage goes dormant and replicates along with the cell. Experimental observations by P. Kourilsky are consistent with a single phage infection deterministically choosing lysis and double infection resulting in a stochastic choice. We argue that the phage are playing a "game" of minimizing the chance of extinction and that the shift from determinism to stochasticity is due to a shift from a single-player to a multiplayer game. Crucial to the argument is the clonal identity of the phage.
Description: Copyright © 2009, American Society for Microbiology. All Rights Reserved.</summary>
    <dc:date>2008-12-31T13:30:00Z</dc:date>
  </entry>
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