The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.
|The Biology of Proteostasis in Aging and Disease v1.0.0||31%|
|Alzheimer’s disease and the autophagic-lysosomal system v1.0.0||31%|
|The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0||23%|
|The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0||23%|
|Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0||23%|
|mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0||15%|
|Heme Curation v0.0.1-dev||15%|
|A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease. v1.0.0||15%|
|A Quantitative Chaperone Interaction Network Reveals the Architecture of Cellular Protein Homeostasis Pathways v1.0.0||15%|
|Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0||15%|
However, CME was substantially reduced in cells con- taining Q82 aggregates (Fig. 1 B , arrows), with quantification of internalized transferrin fluorescence showing a 63 ± 11% reduction in aggregate-containing cells compared with cells expressing soluble Q19 or Q82 (Fig. 1 C ).
CME inhibition was also observed in cells containing aggregated forms of polyQ- expanded Htt exon 1 (Htt Q53); these cells exhibited 50 ± 15% reduced levels of internalized transferrin compared with cells with soluble Htt Q23 or Htt Q53 protein (Fig. S2 A–C ).
It has been proposed that such an imbalance may trigger the onset of many neurodegenerative diseases (10, 26), and recent studies report that polyglutamine (polyQ)-based aggregates can se- quester and inhibit the function of a low-abundance cochaper- one, Sis1p/DNAJB1, in protein degradation (27).
Previous studies have shown that ag- gregation of expanded polyQ negatively affects endocytosis in yeast and in human HEK 293 cells (34).
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.