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Title:          Mutations in SLC39A14 disrupt manganese homeostasis and cause childhood-onset parkinsonism–dystonia
Subject:        Nature Communications 7,  (2016). doi:10.1038/ncomms11601
Author:         Esther Meyer
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       Item: 
        Title: Results
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        Children: 
         Item: 
          Title: SLC39A14 mutations cause Mn-associated neurodegeneration
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         Item: 
          Title: Na2CaEDTA lowers blood Mn and alleviates clinical symptoms
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          Title: Tissue expression and Mn transport differ between isoforms
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          Title: Mn affects transcriptional regulation of zebrafish slc39a14
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         Item: 
          Title: Missense mutations in human SLC39A14 impair Mn uptake
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       Item: 
        Title: Figure™1SLC39A14 mutations lead to cerebral Mn deposition associated with characteristic MRI brain appearances.(a) Schematic of SLC39A14 showing its eight TMDs (pink and blue cylinders) interlinked by intracellular and extracellular loops35. TMD II, III, 
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        Children: 
         Item: 
          Title: slc39a14 loss-of-function causes Mn disturbance in zebrafish
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       Item: 
        Title: Table 1 
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         Item: 
          Title: Cerebral Mn deposition induces transcriptional changes
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       Item: 
        Title: Figure™2SLC39A14 deficiency causes hypermanganesemia and neurodegeneration that responds to chelation treatment with Na2CaEDTA.(a) Liver MRIs of a patient with SLC30A10 deficiency, individual E- II-2 with SLC39A14 mutations and a control subject. The exte
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        Title: Figure™3SLC39A14 isoforms 1 and 2 show differences in tissue expression, Mn uptake and transcriptional regulation.(a) Immunostaining for SLC39A14 (all isoforms) in healthy control liver shows cell membrane expression (yellow arrow) and punctate cytoplasmi
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        Title: Figure™4In vitro expressed mutant SLC39A14 shows compromised Mn uptake despite normal subcellular localization.(a) Immunoblot of whole-cell lysates of stably transfected HEK-293 cells showing expression of the wild-type and three mutant SLC39A14 proteins
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       Item: 
        Title: Figure™5Zebrafish slc39a14 is expressed during early zebrafish development and significantly reduced in slc39a14U801 mutants.(a) RT-PCR showing slc39a14 expression between 3 and 120 hpf in zebrafish. L, 100thinspbp ladder (Promega). (b) Whole-mount in™sit
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        Title: Figure™6Loss of slc39a14 function in zebrafish leads to increased Mn accumulation and sensitivity as well as impaired locomotor behaviour.(a) Mn levels assessed in homozygous slc39a14U801 and wild-type (WT) larvae show that mutant larvae have significantl
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         Item: 
          Title: Na2CaEDTA reduces the Mn load in slc39a14U801 mutants
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       Item: 
        Title: Discussion
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       Item: 
        Title: Figure™7Mn accumulates in the brain of slc39a14U801 mutants and can be lowered by Na2CaEDTA.(a) Tissue Mn levels of wild-type (WT) and homozygous slc39a14U801 zebrafish at 1 year of age show that mutant brain tissue accumulates significantly higher amount
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       Item: 
        Title: Figure™8Proposed disease mechanism in patients with SLC39A14 mutations.(a) Under normal conditions nutritional Mn (red) is absorbed in the duodenum and enters the enterohepatic circulation via the portal vein from which it is transported into the liver vi
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       Item: 
        Title: Methods
        Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@37374a5e
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         Item: 
          Title: Subjects
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          Title: Reagents
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         Item: 
          Title: WES and linkage analysis
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         Item: 
          Title: Variant validation and mutation analysis
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         Item: 
          Title: ICP-MS analysis of metal ions
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@42eca56e
         Item: 
          Title: Histopathology and SLC39A14 immunohistochemistry
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         Item: 
          Title: RNA extraction and qRT-PCR
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         Item: 
          Title: Cloning of human SLC39A14
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         Item: 
          Title: Overexpression of SLC39A14 in zebrafish embryos
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         Item: 
          Title: Transientsolstable transfection of HEK-293 cells
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         Item: 
          Title: Immunofluorescence of HEK-293 cells
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         Item: 
          Title: Immunoblot analysis
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         Item: 
          Title: Zebrafish strains and husbandry
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@64f6106c
         Item: 
          Title: Zebrafish whole-mount in™situ hybridization
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@553a3d88
         Item: 
          Title: 5prime and 3prime RACE of zebrafish slc39a14
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@7a30d1e6
         Item: 
          Title: Generation of zebrafish slc39a14 null mutant
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@5891e32e
         Item: 
          Title: High-resolution melting analysis
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@cb0ed20
         Item: 
          Title: KASP genotyping
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         Item: 
          Title: LC50 determination of MnCl2 in zebrafish larvae
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         Item: 
          Title: Locomotor zebrafish behaviour assay
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         Item: 
          Title: Cardiac injection of Na2CaEDTA
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         Item: 
          Title: Statistical analysis
          Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@32eebfca
       Item: 
        Title: ChenP.ParmaleeN.AschnerM.Genetic factors and manganese-induced neurotoxicityFront. Genet.52652014SantosD.Manganese alters rat brain amino acids levelsBiol. Trace Elem. Res.1503373412012EriksonK. M.ThompsonK.AschnerJ.AschnerM.Manganese neurotoxicity: a foc
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       Item: 
        Title: We would like to thank all patients and families for participation in this study. We thank members of the Wilson, Tada and Rihel labs for help, advice and sharing of reagents, and the UCL fish facility for the excellent zebrafish care. We are thankful to 
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       Item: 
        Title: ACKNOWLEDGEMENTS
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        Title: Author contributions
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       Item: 
        Title: Additional information
        Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@51c8530f
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    Title: Mutations in SLC39A14 disrupt manganese homeostasis and cause childhood-onset parkinsonism–dystonia
    Author: Esther Meyer
    Subject: Nature Communications 7,  (2016). doi:10.1038/ncomms11601
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       Destination: 247
      Annotation: 
       Subtype: Link
       Rect: 105, 231, 110, 237
       Destination: 247
      Annotation: 
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       Rect: 436, 23, 551, 30
     Thumb: true
    Page: 
     Label: 15
     Annotations: 
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      Annotation: 
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     Thumb: true
    Page: 
     Label: 16
     Annotations: 
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       Rect: 406, 678, 528, 685
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     Thumb: true
  Checksum: cdef7860
   Type: CRC32
  Checksum: a01a0fe81d9b4327c590edf1cc3b8b9c
   Type: MD5
  Checksum: 98c1b358d8093d6204e3be7dfcaf29c5736f6acd
   Type: SHA-1