A novel inflammation-induced ubiquitin E3 ligase in alveolar type II cells
- Department of Pediatrics, Mattel Children's Hospital at UCLA and David Geffen School of Medicine at UCLA, Los Angeles, CA (United States)
- Departments of Pathology and Pediatrics, Saint Louis University Health Sciences Center and Cardinal Glennon Children's Hospital, St. Louis, MO (United States)
LINCR was identified as a glucocorticoid-attenuated response gene induced in the lung during endotoxemia. The LINCR protein has structural similarities to Drosophila Neuralized, which regulates the developmentally important Notch signaling pathway. Endotoxemia-induced LINCR expression in vivo was localized by in situ hybridization to alveolar epithelial type II cells, and shown to be induced by LPS and inflammatory cytokines in the T7 alveolar epithelial type II cell line. RING domain-dependent ubiquitin E3 ligase activity of LINCR was demonstrated using full-length FLAG-LINCR or a deletion mutant lacking the RING domain expressed in 293T cells, and using a GST-LINCR RING fusion protein expressed in Escherichia coli. LINCR preferentially interacted with the ubiquitin-conjugating enzyme UbcH6 and preferentially generated polyubiquitin chains linked via non-canonical lysine residues. We conclude that LINCR is a novel inflammation-induced ubiquitin E3 ligase expressed in alveolar epithelial type II cells, and discuss its potential role in the lung response to inflammation.
- OSTI ID:
- 20710866
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 333, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2005.05.102; PII: S0006-291X(05)01059-4; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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