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  • Polyglutamine tracts regulate beclin 1-dependent autophagy 

    Ashkenazi, A; Bento, CF; Ricketts, T; Vicinanza, M; Siddiqi, F; Pavel, M; Squitieri, F et al. (Nature Publishing Group, 2017-05-04)
    Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and ataxin 3 in spinocerebellar ataxia type 3 (SCA3). Age at onset of ...
  • Hypoxia and B cells 

    Burrows, N; Maxwell, PH (Elsevier, 2017-02-27)
    The ability of cells to sense and adapt to changes in oxygen is mediated by hypoxia-inducible factor (HIF). Immune cells function in physiologically complex and varying environments whereby oxygen, pH, nutrients, metabolites ...
  • Mutations in mitochondrial DNA causing tubulointerstitial kidney disease 

    Connor, TM; Hoer, S; Mallett, A; Gale, DP; Gomez Duran, A; Posse, V; Antrobus, R et al. (PLoS, 2017-03-07)
    Tubulointerstitial kidney disease is an important cause of progressive renal failure whose aetiology is incompletely understood. We analysed a large pedigree with maternally inherited tubulointerstitial kidney disease and ...
  • Complement C1q is hydroxylated by collagen prolyl 4 hydroxylase and is sensitive to off-target inhibition by prolyl hydroxylase domain inhibitors that stabilize hypoxia-inducible factor 

    Kiriakidis, S; Hoer, SS; Burrows, N; Biddlecome, G; Khan, MN; Thinnes, CC; Schofield, CJ et al.
    Complement C1q is part of the C1 macromolecular complex that mediates the classical complement activation pathway: a major arm of innate immune defense. C1q is composed of A, B, and C chains that require post-translational ...

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