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001     255139
005     20240112171730.0
024 7 _ |a 10.1038/s41467-023-36553-6
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037 _ _ |a DZNE-2023-00258
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100 1 _ |a Nalbach, Karsten
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245 _ _ |a Spatial proteomics reveals secretory pathway disturbances caused by neuropathy-associated TECPR2.
260 _ _ |a [London]
|c 2023
|b Nature Publishing Group UK
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520 _ _ |a Hereditary sensory and autonomic neuropathy 9 (HSAN9) is a rare fatal neurological disease caused by mis- and nonsense mutations in the gene encoding for Tectonin β-propeller repeat containing protein 2 (TECPR2). While TECPR2 is required for lysosomal consumption of autophagosomes and ER-to-Golgi transport, it remains elusive how exactly TECPR2 is involved in autophagy and secretion and what downstream sequels arise from defective TECPR2 due to its involvement in these processes. To address these questions, we determine molecular consequences of TECPR2 deficiency along the secretory pathway. By employing spatial proteomics, we describe pronounced changes with numerous proteins important for neuronal function being affected in their intracellular transport. Moreover, we provide evidence that TECPR2's interaction with the early secretory pathway is not restricted to COPII carriers. Collectively, our systematic profiling of a HSAN9 cell model points to specific trafficking and sorting defects which might precede autophagy dysfunction upon TECPR2 deficiency.
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650 _ 2 |a Carrier Proteins: metabolism
|2 MeSH
650 _ 2 |a Secretory Pathway
|2 MeSH
650 _ 2 |a Proteomics
|2 MeSH
650 _ 2 |a Protein Transport
|2 MeSH
650 _ 2 |a Autophagosomes
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650 _ 2 |a Autophagy: genetics
|2 MeSH
650 _ 2 |a Golgi Apparatus
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: metabolism
|2 MeSH
650 _ 7 |a Carrier Proteins
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650 _ 7 |a Nerve Tissue Proteins
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700 1 _ |a Schifferer, Martina
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700 1 _ |a Bhattacharya, Debjani
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700 1 _ |a Ho-Xuan, Hung
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700 1 _ |a Tseng, Wei
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700 1 _ |a Williams, Luis A
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700 1 _ |a Stolz, Alexandra
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700 1 _ |a Lichtenthaler, Stefan F
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700 1 _ |a Elazar, Zvulun
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700 1 _ |a Behrends, Christian
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773 _ _ |a 10.1038/s41467-023-36553-6
|g Vol. 14, no. 1, p. 870
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|t Nature Communications
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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