Related references
Note: Only part of the references are listed.Overexpression of Shadoo protein in transgenic mice does not impact the pathogenesis of scrapie
Haiying Wang et al.
NEUROSCIENCE LETTERS (2011)
Down-Regulation of Shadoo in Prion Infections Traces a Pre-Clinical Event Inversely Related to PrPSc Accumulation
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Protease-Resistant Prions Selectively Decrease Shadoo Protein
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Wild-type Shadoo proteins convert to amyloid-like forms under native conditions
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Unexpected Tolerance of α-Cleavage of the Prion Protein to Sequence Variations
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The prion or the related Shadoo protein is required for early mouse embryogenesis
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The α-Secretase-derived N-terminal Product of Cellular Prion, N1, Displays Neuroprotective Function in Vitro and in Vivo
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Evolutionary Descent of Prion Genes from the ZIP Family of Metal Ion Transporters
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Regulation of Embryonic Cell Adhesion by the Prion Protein
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Interactome Analyses Identify Ties of PrPC and Its Mammalian Paralogs to Oligomannosidic N-Glycans and Endoplasmic Reticulum-Derived Chaperones
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Cellular prion protein modulates defensive attention and innate fear-induced behaviour evoked in transgenic mice submitted to an agonistic encounter with the tropical coral snake Oxyrhopus guibei
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Association of a null allele of SPRN with variant Creutzfeldt-Jakob disease
J. A. Beck et al.
JOURNAL OF MEDICAL GENETICS (2008)
The CNS glycoprotein Shadoo has PrPC-like protective properties and displays reduced levels in prion infections
Joel C. Watts et al.
EMBO JOURNAL (2007)
Enhanced susceptibility of Prnp-deficient mice to kainate-induced seizures, neuronal apoptosis, and death:: Role of AMPA/kainate receptors
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JOURNAL OF NEUROSCIENCE RESEARCH (2007)
New molecular insights into cellular survival and stress responses: Neuroprotective role of cellular prion protein (PrPC)
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Neonatal lethality in transgenic mice expressing prion protein with a deletion of residues 105-125
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The C-terminal products of cellular prion protein processing, C1 and C2, exert distinct influence on p53-dependent staurosporine-induced caspase-3 activation
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JOURNAL OF BIOLOGICAL CHEMISTRY (2007)
Mice devoid of prion protein have cognitive deficits that are rescued by reconstitution of PrP in neurons
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Short interfering RNAs can induce unexpected and divergent changes in the levels of untargeted proteins in mammalian cells
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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2004)
The role of PrP in health and disease
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Expression profiling reveals off-target gene regulation by RNAi
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Alzheimer's disease β-amyloid peptide is increased in mice deficient in endothelin-converting enzyme
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Post-natal knockout of prion protein alters hippocampal CA1 properties, but does not result in neurodegeneration
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