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- W2810657526 abstract "Abstract Genetic variants in Granulin (GRN) , which encodes the secreted glycoprotein Progranulin (PGRN), are associated with several neurodegenerative diseases including frontotemporal lobar degeneration, neuronal ceroid lipofuscinosis, and Alzheimer’s disease. These genetic alterations manifest in pathological changes due to a reduction of PGRN expression; therefore, identifying a factor that can modulate PGRN levels in vivo would enhance our understanding of PGRN in neurodegeneration, and could reveal novel potential therapeutic targets. Here, we report that Nemo-like kinase (Nlk) regulates Pgrn levels and its associated neuropathophysiology. Genetic interaction studies in mice show that Grn heterozygote mice on an Nlk heterozygote background display pathological and behavioral phenotypes which mimic Grn knockout mice. Furthermore, biochemical and cell biological studies suggest that Nlk reduction promotes Pgrn degradation via the endocytosis-lysosomal pathway, specifically in microglia. Our results reveal a new mechanism for the regulation of Pgrn in the brain and provide insight into the pathophysiology of PGRN-associated diseases." @default.
- W2810657526 created "2018-07-10" @default.
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- W2810657526 date "2018-06-28" @default.
- W2810657526 modified "2023-09-22" @default.
- W2810657526 title "Nemo-like kinase regulates Progranulin levels in the brain through the microglial endocytosis-lysosomal pathway" @default.
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- W2810657526 doi "https://doi.org/10.1101/358010" @default.
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