Sippl, Christiane and Zeilbeck, Ludwig F. and Fuchshofer, Rudolf and Tamm, Ernst R. (2014) Optineurin associates with the podocyte Golgi complex to maintain its structure. CELL AND TISSUE RESEARCH, 358 (2). pp. 567-583. ISSN 0302-766X, 1432-0878
Full text not available from this repository. (Request a copy)Abstract
Optineurin, a cytosolic protein associated with the actin cytoskeleton, microtubules, and the Golgi complex, appears to have an important function in neurons, as mutations in its gene are causative for neurodegenerative diseases such as primary open-angle glaucoma and amyotrophic lateral sclerosis. Here, we report that optineurin is localized in podocytes of the kidney and induced upon injury following treatment with puromycin aminonucleoside. In cultured human podocytes, optineurin localizes to the Golgi complex. Optineurin depletion by RNA interference causes Golgi fragmentation. Moreover, if the Golgi complex is fragmented following microtubule destabilization induced by nocodazole treatment, optineurin dissociates from Golgi vesicles. Furthermore, optineurin colocalizes with vinculin-labeled focal contacts of cultured podocytes and with lysosome-like structures. Optineurin is essential for the survival of cultured podocytes, as optineurin depletion causes cell death. Thus, optineurin appears to play an important role in the maintenance of the podocyte Golgi complex and in the trafficking of vesicles to focal contacts and lysosomes.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | NF-KAPPA-B; AMYOTROPHIC-LATERAL-SCLEROSIS; EXPRESSION; PROTEIN; HUNTINGTIN; GLAUCOMA; PATHWAY; CELLS; PHOSPHORYLATION; LOCALIZATION; Optineurin; Golgi complex; Focal contact; Podocyte; Minimal change nephrosis |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Anatomie > Lehrstuhl für Humananatomie und Embryologie > Prof. Dr. Ernst Tamm |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 08 Aug 2019 10:35 |
| Last Modified: | 08 Aug 2019 10:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/9293 |
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