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- W2000504008 endingPage "e0118956" @default.
- W2000504008 startingPage "e0118956" @default.
- W2000504008 abstract "Loss of function mutations in granulin (GRN) are linked to two distinct neurological disorders, frontotemporal lobar degeneration (FTLD) and neuronal ceroid lipofuscinosis (NCL). It is so far unknown how a complete loss of GRN in NCL and partial loss of GRN in FTLD can result in such distinct diseases. In zebrafish, there are two GRN homologues, Granulin A (Grna) and Granulin B (Grnb). We have generated stable Grna and Grnb loss of function zebrafish mutants by zinc finger nuclease mediated genome editing. Surprisingly, the grna and grnb single and double mutants display neither spinal motor neuron axonopathies nor a reduced number of myogenic progenitor cells as previously reported for Grna and Grnb knock down embryos. Additionally, grna−/−;grnb−/− double mutants have no obvious FTLD- and NCL-related biochemical and neuropathological phenotypes. Taken together, the Grna and Grnb single and double knock out zebrafish lack any obvious morphological, pathological and biochemical phenotypes. Loss of zebrafish Grna and Grnb might therefore either be fully compensated or only become symptomatic upon additional challenge." @default.
- W2000504008 created "2016-06-24" @default.
- W2000504008 creator A5007055980 @default.
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- W2000504008 creator A5065084452 @default.
- W2000504008 creator A5065576952 @default.
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- W2000504008 date "2015-03-18" @default.
- W2000504008 modified "2023-10-16" @default.
- W2000504008 title "Granulin Knock Out Zebrafish Lack Frontotemporal Lobar Degeneration and Neuronal Ceroid Lipofuscinosis Pathology" @default.
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- W2000504008 doi "https://doi.org/10.1371/journal.pone.0118956" @default.
- W2000504008 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4365039" @default.
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- W2000504008 hasPublicationYear "2015" @default.
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